IP Library › Granted Patent US 12,441,785
Granted Patent B2
US 12,441,785 · App. 15/013,008 · Granted Oct 14, 2025

Methods of treating inflammatory diseases

Inventors: Matthias Arndt (Laupheim, DE); Stella Aslanyan (Danbury, CT); Mary Ruth Flack (Ridgefield, CT); Annette Bettina Galler (Armsheim, DE); Bojan Lalovic (Cedar Knolls, NJ); Steven John Padula (Southbury, CT); Paul Russell Scholl (Redding, CT)
Assignee: Boehringer Ingelheim International GmbH
C07K16/244A61K2039/505A61K2039/545C07K2317/76
View Patent ↗
Loading inventors, assignments & file history…
Monitor This Case
Get email alerts when status or documents change.
Order Certified Copies
Most orders are placed with the USPTO same day — all within 24 business hours.
Order via The Patent Place →
Pre-filled with this patent's details
Quick Facts
Patent No.
US 12,441,785
App. No.
15/013,008
Granted
Oct 14, 2025
Kind
B2
Abstract

This invention generally relates to methods for the treatment of IL-23 related diseases, in particular inflammatory diseases, such as psoriasis, psoriatic arthritis or axial (spinal) spondyloarthritis (ax-SpA), including ankylosing spondylitis and non-radiographic ax-SpA, utilizing anti-IL-23A antibodies.

Claims (183)

1. A method for treating moderate to severe plaque psoriasis in an adult human patient with moderate to severe plaque psoriasis, comprising administering to the patient a safe and therapeutically effective dosing regimen of a full-length anti-IL-23A antibody, said anti-IL-23A antibody comprising two light chains each having the amino acid sequence of SEQ ID NO: 18 and two heavy chains each having the amino acid sequence of SEQ ID NO: 19, wherein said treating is significantly reducing or completely clearing psoriatic skin lesions, the dosing regimen comprising:

a) subcutaneously administering to the patient a first dose of 150 mg of said anti-IL-23A antibody regardless of the patient's body weight; and

b) subcutaneously administering to the patient a second dose of 150 mg of said anti-IL-23A antibody regardless of the patient's body weight 4 weeks after said first dose is administered,

wherein the method results in the patient achieving at least a 90% reduction from baseline Psoriasis Area and Severity Index score (PASI 90) 12 weeks after receiving the first dose.

2. The method according to claim 1 , wherein each of the 150 mg doses is administered as two 75 mg subcutaneous injections.

3. A method for treating scalp psoriasis in an adult human patient with scalp psoriasis, comprising administering to the patient a safe and therapeutically effective dosing regimen of a full-length anti-IL-23A antibody, said anti-IL-23A antibody comprising two light chains each having the amino acid sequence of SEQ ID NO:18 and two heavy chains each having the amino acid sequence of SEQ ID NO:19, wherein said treating is completely clearing scalp psoriasis, the dosing regimen comprising:

a) subcutaneously administering to the patient a first dose of 150 mg of said anti-IL-23A antibody regardless of the patient's body weight; and

b) subcutaneously administering to the patient a second dose of 150 mg of said anti-IL-23A antibody regardless of the patient's body weight 4 weeks after said first dose is administered,

wherein the method results in the patient achieving complete clearance of scalp psoriasis as measured by Psoriasis Scalp Severity Index (PSSI) 6 weeks after receiving the first dose.

4. A method for treating palmoplantar psoriasis in an adult human patient with palmoplantar, psoriasis comprising administering to the patient a safe and therapeutically effective dosing regimen of a full-length anti-IL-23A antibody, said anti-IL-23A antibody comprising two light chains each having the amino acid sequence of SEQ ID NO:18 and two heavy chains each having the amino acid sequence of SEQ ID NO:19, wherein said treating is completely clearing palmoplantar psoriasis, the dosing regimen comprising:

a) subcutaneously administering to the patient a first dose of 150 mg of said anti-IL-23A antibody regardless of the patient's body weight; and

b) subcutaneously administering to the patient a second dose of 150 mg of said anti-IL-23A antibody regardless of the patient's body weight 4 weeks after said first dose is administered,

wherein the method results in the patient achieving complete clearance of palmoplantar psoriasis as measured by Palmoplantar Psoriasis Area Severity Index (PPASI) 6 weeks after receiving the first dose.

5. A method for treating nail psoriasis in an adult human patient with nail psoriasis comprising administering to the patient a safe and therapeutically effective dosing regimen of a full-length anti-IL-23A antibody, said anti-IL-23A antibody comprising two light chains each having the amino acid sequence of SEQ ID NO: 18 and two heavy chains each having the amino acid sequence of SEQ ID NO:19, wherein said treating is significantly reducing the severity of nail psoriasis, the dosing regimen comprising:

a) subcutaneously administering to the patient a first dose of 150 mg of said anti-IL-23A antibody regardless of the patient's body weight; and

b) subcutaneously administering to the patient a second dose of 150 mg of said anti-IL-23A antibody regardless of the patient's body weight 4 weeks after said first dose is administered,

wherein the method results in the patient achieving an improvement from baseline Nail Psoriasis Severity Index (NAPSI) 6 weeks after receiving the first dose.

6. The method according to claim 3 , wherein each of the 150 mg doses is administered as two 75 mg subcutaneous injections.

7. The method according to claim 4 , wherein each of the 150 mg doses is administered as two 75 mg subcutaneous injections.

8. The method according to claim 5 , wherein each of the 150 mg doses is administered as two 75 mg subcutaneous injections.

9. A method for treating psoriatic arthritis in an adult human patient with psoriatic arthritis, comprising administering to the patient a safe and therapeutically effective dosing regimen of a full-length anti-IL-23A antibody, said anti-IL-23A antibody comprising two light chains each having the amino acid sequence of SEQ ID NO:18 and two heavy chains each having the amino acid sequence of SEQ ID NO:19, wherein said treating is improving one or more measures of psoriatic arthritis disease activity, the dosing regimen comprising:

a) subcutaneously administering to the patient a first dose of 150 mg of said anti-IL-23A antibody regardless of the patient's body weight; and

b) subcutaneously administering to the patient a second dose of 150 mg of said anti-IL-23A antibody regardless of the patient's body weight 4 weeks after said first dose is administered,

wherein the method results in the patient achieving at least a 50% improvement in American College of Rheumatology response criteria (ACR 50) 24 weeks after receiving the first dose.

10. A method for treating moderate to severe plaque psoriasis in an adult human patient having moderate to severe plaque psoriasis, comprising administering to the patient a safe and therapeutically effective dosing regimen of a full-length anti-IL-23A antibody, said anti-IL-23A antibody comprising two light chains each having the amino acid sequence of SEQ ID NO:18 and two heavy chains each having the amino acid sequence of SEQ ID NO:19, wherein said treating is significantly reducing or completely clearing psoriatic skin lesions, the dosing regimen comprising:

a) subcutaneously administering to the patient a first dose of 150 mg of said anti-IL-23A antibody regardless of the patient's body weight;

b) subcutaneously administering to the patient a second dose of 150 mg of said anti-IL-23A antibody regardless of the patient's body weight 4 weeks after said first dose is administered; and

c) subcutaneously administering to the patient a third dose of 150 mg of said anti-IL-23A antibody regardless of the patient's body weight 12 weeks after said second dose is administered,

wherein the method results in the patient achieving at least a 90% reduction from baseline Psoriasis Area and Severity Index score (PASI 90) 16 weeks after receiving the first dose.

11. A method for treating scalp psoriasis in an adult human patient with scalp psoriasis, comprising administering to the patient a safe and therapeutically effective dosing regimen of a full-length anti-IL-23A antibody, said anti-IL-23A antibody comprising two light chains each having the amino acid sequence of SEQ ID NO:18 and two heavy chains each having the amino acid sequence of SEQ ID NO: 19, wherein said treating is completely clearing scalp psoriasis, the dosing regimen comprising:

a) subcutaneously administering to the patient a first dose of 150 mg of said anti-IL-23A antibody regardless of the patient's body weight;

b) subcutaneously administering to the patient a second dose of 150 mg of said anti-IL-23A antibody regardless of the patient's body weight 4 weeks after said first dose is administered; and

c) subcutaneously administering to the patient a third dose of 150 mg of said anti-IL-23A antibody regardless of the patient's body weight 12 weeks after said second dose is administered,

wherein the method results in the patient achieving complete clearance of scalp psoriasis as measured by Psoriasis Scalp Severity Index (PSSI) 6 weeks after receiving the first dose.

12. A method for treating palmoplantar psoriasis in an adult human patient with palmoplantar psoriasis, comprising administering to the patient a safe and therapeutically effective dosing regimen of a full-length anti-IL-23A antibody, said anti-IL-23A antibody comprising two light chains each having the amino acid sequence of SEQ ID NO:18 and two heavy chains each having the amino acid sequence of SEQ ID NO:19, wherein said treating is completely clearing palmoplantar psoriasis, the dosing regimen comprising:

a) subcutaneously administering to the patient a first dose of 150 mg of said anti-IL-23A antibody regardless of the patient's body weight; and

b) subcutaneously administering to the patient a second dose of 150 mg of said anti-IL-23A antibody regardless of the patient's body weight 4 weeks after said first dose is administered, and c) subcutaneously administering to the patient a third dose of 150 mg of said anti-IL-23A antibody regardless of the patient's body weight 12 weeks after said second dose is administered,

wherein the method results in the patient achieving complete clearance of palmoplantar psoriasis as measured by Palmoplantar Psoriasis Area Severity Index (PPASI) 6 weeks after receiving the first dose.

13. A method for treating nail psoriasis in an adult human patient with nail psoriasis, comprising administering to the patient a safe and therapeutically effective dosing regimen of a full-length anti-IL-23A antibody, said anti-IL-23A antibody comprising two light chains each having the amino acid sequence of SEQ ID NO:18 and two heavy chains each having the amino acid sequence of SEQ ID NO:19, wherein said treating is significantly reducing the severity of nail psoriasis, the dosing regimen comprising:

a) subcutaneously administering to the patient a first dose of 150 mg of said anti-IL-23A antibody regardless of the patient's body weight; and

b) subcutaneously administering to the patient a second dose of 150 mg of said anti-IL-23A antibody regardless of the patient's body weight 4 weeks after said first dose is administered, and c) subcutaneously administering to the patient a third dose of 150 mg of said anti-IL-23A antibody regardless of the patient's body weight 12 weeks after said second dose is administered,

wherein the method results in the patient achieving an improvement from baseline Nail Psoriasis Severity Index (NAPSI) 6 weeks after receiving the first dose.

14. A method for treating psoriatic arthritis in an adult human patient with psoriatic arthritis, comprising administering to the patient a safe and therapeutically effective dosing regimen of a full-length anti-IL-23A antibody, said anti-IL-23A antibody comprising two light chains each having the amino acid sequence of SEQ ID NO:18 and two heavy chains each having the amino acid sequence of SEQ ID NO:19, wherein said treating is improving one or more measures of psoriatic arthritis disease activity, the dosing regimen comprising:

a) subcutaneously administering to the patient a first dose of 150 mg of said anti-IL-23A antibody regardless of the patient's body weight; and

b) subcutaneously administering to the patient a second dose of 150 mg of said anti-IL-23A antibody regardless of the patient's body weight 4 weeks after said first dose is administered, c) subcutaneously administering to the patient a third dose of 150 mg of said anti-IL-23A antibody regardless of the patient's body weight 12 weeks after said second dose is administered,

wherein the method results in the patient achieving at least a 50% improvement in American College of Rheumatology response criteria (ACR 50) 24 weeks after receiving the first dose.

15. The method according to claim 10 , wherein beginning 12 weeks after the third dose is administered to the patient, a dose of 150 mg of the anti-IL-23A antibody is subcutaneously administered to the patient regardless of the patient's body weight once every 12 weeks.

16. The method according to claim 11 , wherein beginning 12 weeks after the third dose is administered to the patient, a dose of 150 mg of the anti-IL 23A antibody is subcutaneously administered to the patient regardless of the patient's body weight once every 12 weeks.

17. The method according to claim 12 , wherein beginning 12 weeks after the third dose is administered to the patient, a dose of 150 mg of the anti-IL-23A antibody is subcutaneously administered to the patient regardless of the patient's body weight once every 12 weeks.

18. The method according to claim 13 , wherein beginning 12 weeks after the third dose is administered to the patient, a dose of 150 mg of the anti-IL-23A antibody is subcutaneously administered to the patient regardless of the patient's body weight once every 12 weeks.

19. The method according to claim 14 , wherein beginning 12 weeks after the third dose is administered to the patient, a dose of 150 mg of the anti-IL-23A antibody is subcutaneously administered to the patient regardless of the patient's body weight once every 12 weeks.

20. The method according to claim 9 , wherein each of the 150 mg doses is administered as two 75 mg subcutaneous injections.

21. The method according to claim 10 , wherein each of the 150 mg doses is administered as two 75 mg subcutaneous injections.

22. The method according to claim 11 , wherein each of the 150 mg doses is administered as two 75 mg subcutaneous injections.

23. The method according to claim 12 , wherein each of the 150 mg doses is administered as two 75 mg subcutaneous injections.

24. The method according to claim 13 , wherein each of the 150 mg doses is administered as two 75 mg subcutaneous injections.

25. The method according to claim 14 , wherein each of the 150 mg doses is administered as two 75 mg subcutaneous injections.

26. The method according to claim 1 , wherein the method results in a 100% reduction from baseline Psoriasis Area and Severity Index score (PASI 100) 16 weeks after receiving the first dose.

27. The method according to claim 10 , wherein the method results in a 100% reduction from baseline Psoriasis Area and Severity Index score (PASI 100) 16 weeks after receiving the first dose.

28. The method according to claim 9 , wherein the method results in the patient achieving at least a 50% improvement in American College of Rheumatology response criteria (ACR 50) 16 weeks after receiving the first dose.

29. The method according to claim 9 , wherein the method results in the patient achieving at least a 70% improvement in American College of Rheumatology response criteria (ACR 70) 24 weeks after receiving the first dose.

30. The method according to claim 9 , wherein the method results in the patient achieving at least a 70% improvement in American College of Rheumatology response criteria (ACR 70) 16 weeks after receiving the first dose.

31. The method according to claim 14 , wherein the method results in the patient achieving at least a 50% improvement in American College of Rheumatology response criteria (ACR 50) 16 weeks after receiving the first dose.

32. The method according to claim 14 , wherein the method results in the patient achieving at least a 70% improvement in American College of Rheumatology response criteria (ACR 70) 24 weeks after receiving the first dose.

33. The method according to claim 14 , wherein the method results in the patient achieving at least a 70% improvement in American College of Rheumatology response criteria (ACR 70) 16 weeks after receiving the first dose.

34. The method according to claim 1 , wherein the method results in the patient achieving a Static Physician Global Assessment (sPGA) score of 0 or 1at 12 weeks after receiving the first dose.

35. A method for treating moderate to severe plaque psoriasis in an adult human patient with moderate to severe plaque psoriasis, comprising administering to the patient a safe and therapeutically effective dosing regimen of a full-length anti-IL-23A antibody, said anti-IL-23A antibody comprising two light chains each having the amino acid sequence of SEQ ID NO:18 and two heavy chains each having the amino acid sequence of SEQ ID NO:19, wherein said treating is significantly reducing or completely clearing psoriatic skin lesions, the dosing regimen comprising:

a) subcutaneously administering to the patient a first dose of 90 mg to 180 mg of said anti-IL-23A antibody regardless of the patient's body weight; and

b) subcutaneously administering to the patient a second dose of said anti-IL-23A antibody 4 weeks after said first dose is administered,

wherein the second dose comprises an amount of the anti-IL-23A antibody equal to the first dose regardless of the patients' body weight, and wherein the method results in the patient achieving at least a 90% reduction from baseline Psoriasis Area and Severity Index score (PASI 90) 12 weeks after receiving the first dose.

36. The method according to claim 35 , wherein each of the first and second doses is administered as two subcutaneous injections, wherein each of the subcutaneous injections delivers an equal amount of the anti-IL-23A antibody to the patient.

37. A method for treating scalp psoriasis in an adult human patient with scalp psoriasis, comprising administering to the patient a safe and therapeutically effective dosing regimen of a full-length anti-IL-23A antibody, said anti-IL-23A antibody comprising two light chains each having the amino acid sequence of SEQ ID NO: 18 and two heavy chains each having the amino acid sequence of SEQ ID NO:19, wherein said treating is completely clearing scalp psoriasis, the dosing regimen comprising:

a) subcutaneously administering to the patient a first dose of 90 mg to 180 mg of said anti-IL-23A antibody regardless of the patient's body weight; and

b) subcutaneously administering to the patient a second dose of said anti-IL-23A antibody 4 weeks after said first dose is administered,

wherein the second dose comprises an amount of the anti-IL-23A antibody equal to the first dose regardless of the patient's body weight, and wherein the method results in the patient achieving complete clearance of scalp psoriasis as measured by Psoriasis Scalp Severity Index (PSSI) 6 weeks after receiving the first dose.

38. The method according to claim 37 , wherein each of the first and second doses is administered as two subcutaneous injections, wherein each of the subcutaneous injections delivers an equal amount of the anti-IL-23A antibody to the patient.

39. A method for treating palmoplantar psoriasis in an adult human patient with palmoplantar psoriasis, comprising administering to the patient a safe and therapeutically effective dosing regimen of a full-length anti-IL-23A antibody, said anti-IL-23A antibody comprising two light chains each having the amino acid sequence of SEQ ID NO:18 and two heavy chains each having the amino acid sequence of SEQ ID NO: 19, wherein said treating is completely clearing palmoplantar psoriasis, the dosing regimen comprising:

a) subcutaneously administering to the patient a first dose of 90 mg to 180 mg of said anti-IL-23A antibody regardless of the patient's body weight; and

b) subcutaneously administering to the patient a second dose of said anti-IL-23A antibody 4 weeks after said first dose is administered,

wherein the second dose comprises an amount of the anti-IL-23A antibody equal to the first dose regardless of the patient's body weight, and wherein the method results in the patient achieving complete clearance of palmoplantar psoriasis as measured by Palmoplantar Psoriasis Area Severity Index (PPASI) 6 weeks after receiving the first dose.

40. The method according to claim 39 , wherein each of the first and second doses is administered as two subcutaneous injections, wherein each of the subcutaneous injections delivers an equal amount of the anti-IL-23A antibody to the patient.

41. A method for treating nail psoriasis in an adult human patient with nail psoriasis, comprising administering to the patient a safe and therapeutically effective dosing regimen of a full-length anti-IL-23A antibody, said anti-IL-23A antibody comprising two light chains each having the amino acid sequence of SEQ ID NO: 18 and two heavy chains each having the amino acid sequence of SEQ ID NO:19, wherein said treating is significantly reducing nail psoriasis, the dosing regimen comprising:

a) subcutaneously administering to the patient a first dose of 90 mg to 180 mg of said anti-IL-23A antibody regardless of the patient's body weight; and

b) subcutaneously administering to the patient a second dose of said anti-IL-23A antibody 4 weeks after said first dose is administered,

wherein the second dose comprises an amount of the anti-IL-23A antibody equal to the first dose regardless of the patient's body weight, and wherein the method results in the patient achieving an improvement from baseline Nail Psoriasis Severity Index (NAPSI) 6 weeks after receiving the first dose.

42. The method according to claim 41 , wherein each of the first and second doses is administered as two subcutaneous injections, wherein each of the subcutaneous injections delivers an equal amount of the anti-IL-23A antibody to the patient.

43. A method for treating psoriatic arthritis in an adult human patient with psoriatic arthritis, comprising administering to the patient a safe and therapeutically effective dosing regimen of a full-length anti-IL-23A antibody, said anti-IL-23A antibody comprising two light chains each having the amino acid sequence of SEQ ID NO:18 and two heavy chains each having the amino acid sequence of SEQ ID NO:19, wherein said treating is improving one or more measures of psoriatic arthritis disease activity, the dosing regimen comprising:

a) subcutaneously administering to the patient a first dose of 90 mg to 180 mg of said anti-IL-23A antibody regardless of the patient's body weight; and

b) subcutaneously administering to the patient a second dose of said anti-IL-23A antibody 4 weeks after said first dose is administered,

wherein the second dose comprises an amount of the anti-IL-23A antibody equal to the first dose regardless of the patient's body weight, and wherein the method results in the patient achieving at least a 50% improvement in American College of Rheumatology response criteria (ACR 50) 24 weeks after receiving the first dose.

44. The method according to claim 43 , wherein each of the first and second doses is administered as two subcutaneous injections, wherein each of the subcutaneous injections delivers an equal amount of the anti-IL-23A antibody to the patient.

45. A method for treating moderate to severe plaque psoriasis in an adult human patient with moderate to severe plaque psoriasis, comprising administering to the patient a safe and therapeutically effective dosing regimen of a full-length anti-IL-23A antibody, said anti-IL-23A antibody comprising two light chains each having the amino acid sequence of SEQ ID NO:18 and two heavy chains each having the amino acid sequence of SEQ ID NO:19, wherein said treating is significantly reducing or completely clearing psoriatic skin lesions, the dosing regimen comprising:

a) subcutaneously administering to the patient a first dose of 90 mg to 180 mg of said anti-IL-23A antibody regardless of the patient's body weight;

b) subcutaneously administering to the patient a second dose of said anti-IL-23A antibody 4 weeks after said first dose is administered; and

c) subcutaneously administering to the patient a third dose of said anti-IL-23A antibody 12 weeks after said second dose is administered,

wherein the second dose and the third dose each comprise an amount of the anti-IL-23A antibody equal to the first dose regardless of the patient's body weight, and wherein the method results in the patient achieving at least a 90% reduction from baseline Psoriasis Area and Severity Index score (PASI 90) 16 weeks after receiving the first dose.

46. A method for treating scalp psoriasis in an adult human patient with scalp psoriasis, comprising administering to the patient a safe and therapeutically effective dosing regimen of a full-length anti-IL-23A antibody, said anti-IL-23A antibody comprising two light chains each having the amino acid sequence of SEQ ID NO:18 and two heavy chains each having the amino acid sequence of SEQ ID NO:19, wherein said treating is completely clearing scalp psoriasis, the dosing regimen comprising:

a) subcutaneously administering to the patient a first dose of 90 mg to 180 mg of said anti-IL-23A antibody regardless of the patient's body weight;

b) subcutaneously administering to the patient a second dose of said anti-IL-23A antibody 4 weeks after said first dose is administered; and

c) subcutaneously administering to the patient a third dose of said anti-IL-23A antibody 12 weeks after said second dose is administered,

wherein the second dose and the third dose each comprise an amount of the anti-IL-23A antibody equal to the first dose regardless of the patient's body weight, and wherein the method results in the patient achieving complete clearance of scalp psoriasis as measured by Psoriasis Scalp Severity Index (PSSI) 6 weeks after receiving the first dose.

47. A method for treating palmoplantar psoriasis in an adult human patient with palmoplantar psoriasis, comprising administering to the patient a safe and therapeutically effective dosing regimen of a full-length anti-IL-23A antibody, said anti-IL-23A antibody comprising two light chains each having the amino acid sequence of SEQ ID NO:18 and two heavy chains each having the amino acid sequence of SEQ ID NO: 19, wherein said treating is completely clearing palmoplantar psoriasis, the dosing regimen comprising:

a) subcutaneously administering to the patient a first dose of 90 mg to 180 mg of said anti-IL-23A antibody regardless of the patient's body weight;

b) subcutaneously administering to the patient a second dose of said anti-IL-23A antibody 4 weeks after said first dose is administered; and

c) subcutaneously administering to the patient a third dose of said anti-IL-23A antibody 12 weeks after said second dose is administered,

wherein the second dose and the third dose each comprise an amount of the anti-IL-23A antibody equal to the first dose regardless of the patient's body weight and wherein the method results in the patient achieving complete clearance of palmoplantar psoriasis as measured by Palmoplantar Psoriasis Area Severity Index (PPASI) 6 weeks after receiving the first dose.

48. A method for treating nail psoriasis in an adult human patient with nail psoriasis, comprising administering to the patient a safe and therapeutically effective dosing regimen of a full-length anti-IL-23A antibody, said anti-IL-23A antibody comprising two light chains each having the amino acid sequence of SEQ ID NO:18 and two heavy chains each having the amino acid sequence of SEQ ID NO: 19, wherein said treating is significantly reducing the severity of nail psoriasis, the dosing regimen comprising:

a) subcutaneously administering to the patient a first dose of 90 mg to 180 mg of said anti-IL-23A antibody regardless of the patient's body weight;

b) subcutaneously administering to the patient a second dose of said anti-IL-23A antibody 4 weeks after said first dose is administered; and

c) subcutaneously administering to the patient a third dose of said anti-IL-23A antibody 12 weeks after said second dose is administered,

wherein the second dose and the third dose each comprise an amount of the anti-IL-23A antibody equal to the first dose regardless of the patient's body weight and wherein the method results in the patient achieving an improvement from baseline Nail Psoriasis Severity Index (NAPSI) 6 weeks after receiving the first dose.

49. A method for treating psoriatic arthritis in an adult human patient with psoriatic arthritis, comprising administering to the patient a safe and therapeutically effective dosing regimen of a full-length anti-IL-23A antibody, said anti-IL-23A antibody comprising two light chains each having the amino acid sequence of SEQ ID NO:18 and two heavy chains each having the amino acid sequence of SEQ ID NO: 19, wherein said treating is improving one or more measures of psoriatic arthritis disease activity, the dosing regimen comprising:

a) subcutaneously administering to the patient a first dose of 90 mg to 180 mg of said anti-IL-23A antibody regardless of the patient's body weight;

b) subcutaneously administering to the patient a second dose of said anti-IL-23A antibody 4 weeks after said first dose is administered; and

c) subcutaneously administering to the patient a third dose of said anti-IL-23A antibody 12 weeks after said second dose is administered,

wherein the second dose and the third dose each comprise an amount of the anti-IL-23A antibody equal to the first dose regardless of the patient's body weight and wherein the method results in the patient achieving at least a 50% improvement in American College of Rheumatology response criteria (ACR 50) 24 weeks after receiving the first dose.

50. The method according to claim 45 , wherein beginning 12 weeks after the third dose is administered to the patient, additional doses of the anti-IL-23A antibody are subcutaneously administered to the patient once every 12 weeks, and wherein said additional doses each comprise an amount of the anti-IL-23 antibody equal to the first dose regardless of the patient's body weight.

51. The method according to claim 46 , wherein beginning 12 weeks after the third dose is administered to the patient, additional doses of the anti-IL-23A antibody are subcutaneously administered to the patient once every 12 weeks, and wherein said additional doses each comprise an amount of the anti-IL-23 antibody equal to the first dose regardless of the patient's body weight.

52. The method according to claim 47 , wherein beginning 12 weeks after the third dose is administered to the patient, a additional doses of the anti-IL-23A antibody are subcutaneously administered to the patient once every 12 weeks, and wherein said additional doses each comprise an amount of the anti-IL-23 antibody equal to the first dose regardless of the patient's body weight.

53. The method according to claim 48 , wherein beginning 12 weeks after the third dose is administered to the patient, a additional doses of the anti-IL-23A antibody are subcutaneously administered to the patient once every 12 weeks, and wherein said additional doses each comprise an amount of the anti-IL-23 antibody equal to the first dose regardless of the patient's body weight.

54. The method according to claim 49 , wherein beginning 12 weeks after the third dose is administered to the patient, additional doses of the anti-IL-23A antibody are subcutaneously administered to the patient once every 12 weeks, and wherein said additional doses each comprise an amount of the anti-IL-23 antibody equal to the first dose regardless of the patient's body weight.

55. A method for treating psoriatic arthritis in an adult human patient with psoriatic arthritis, comprising administering to the patient a safe and therapeutically effective dosing regimen of a full-length anti-IL-23A antibody, said anti-IL-23A antibody comprising two light chains each having the amino acid sequence of SEQ ID NO: 18 and two heavy chains each having the amino acid sequence of SEQ ID NO: 19, wherein said treating is improving one or more measures of psoriatic arthritis disease activity, the dosing regimen comprising:

a) subcutaneously administering to the patient a first dose of 150 mg of said anti-IL-23A antibody regardless of the patient's body weight; and

b) subcutaneously administering to the patient a second dose of 150 mg of said anti-IL-23A antibody regardless of the patient's body weight 4 weeks after said first dose is administered;

wherein the method results in the patient achieving at least a 50% reduction from baseline in pain as assessed by Visual Analog Scale score at 12 weeks after receiving the first dose.

56. A method for treating psoriatic arthritis in an adult human patient with psoriatic arthritis, comprising administering to the patient a safe and therapeutically effective dosing regimen of a full-length anti-IL-23A antibody, said anti-IL-23A antibody comprising two light chains each having the amino acid sequence of SEQ ID NO:18 and two heavy chains each having the amino acid sequence of SEQ ID NO: 19, wherein said treating is improving one or more measures of psoriatic arthritis disease activity, the dosing regimen comprising:

a) subcutaneously administering to the patient a first dose of 90 mg to 180 mg of said anti-IL-23A antibody regardless of the patient's body weight; and

b) subcutaneously administering to the patient a second dose of said anti-IL-23A antibody 4 weeks after said first dose is administered;

wherein the second dose comprises an amount of the anti-IL-23A antibody equal to the first dose regardless of the patient's body weight, and wherein the method results in the patient achieving at least a 50% reduction from baseline in pain as assessed by Visual Analog Scale score at 12 weeks after receiving the first dose.

57. A method for treating moderate to severe plaque psoriasis, comprising administering to a human patient with moderate to severe plaque psoriasis a therapeutically effective dosing regimen of a full-length anti-IL-23A antibody, said anti-IL-23A antibody comprising two light chains each having the amino acid sequence of SEQ ID NO:18 and two heavy chains each having the amino acid sequence of SEQ ID NO:19, wherein said treating is significantly reducing or completely clearing psoriatic skin lesions, the dosing regimen comprising:

a) subcutaneously administering to the patient a first dose of 150 mg of said anti-IL-23A antibody regardless of the patient's body weight; and

b) subcutaneously administering to the patient a second dose of 150 mg of said anti-IL-23A antibody regardless of the patient's body weight 4 weeks after said first dose is administered,

wherein the method results in the patient achieving a Static Physician Global Assessment (sPGA) score of 0 or 1 at 12 weeks after receiving the first dose.

58. The method according to claim 57 , wherein beginning 12 weeks after the second dose is administered to the patient, a dose of 150 mg of the anti-IL-23A antibody is subcutaneously administered to the patient regardless of the patient's body weight once every 12 weeks.

59. A method for treating moderate to severe plaque psoriasis, comprising administering to a human patient with moderate to severe plaque psoriasis a therapeutically effective dosing regimen of a full-length anti-IL-23A antibody, said anti-IL-23A antibody comprising two light chains each having the amino acid sequence of SEQ ID NO:18 and two heavy chains each having the amino acid sequence of SEQ ID NO: 19, wherein said treating is significantly reducing or completely clearing psoriatic skin lesions, the dosing regimen comprising:

a) subcutaneously administering to the patient a first dose of 90 mg to 180 mg of said anti-IL-23A antibody regardless of the patient's body weight; and

b) subcutaneously administering to the patient a second dose of said anti-IL-23A antibody 4 weeks after said first dose is administered,

wherein the second dose comprises an amount of the anti-IL-23A antibody equal to the first dose regardless of the patient's body weight, and wherein the method results in the patient achieving a Static Physician Global Assessment (sPGA) score of 0 or 1 at 12 weeks after receiving the first dose.

60. The method according to claim 59 , wherein beginning 12 weeks after the second dose is administered to the patient, additional doses of the anti-IL-23A antibody are subcutaneously administered to the patient once every 12 weeks and wherein said additional doses each comprise an amount of the anti-IL-23A antibody equal to the first dose regardless of the patient's body weight.

61. A method of treating palmoplantar psoriasis, comprising administering to a human patient with palmoplantar psoriasis a therapeutically effective dosing regimen of a full-length anti-IL-23A antibody, said anti-IL-23A antibody comprising two light chains each having the amino acid sequence of SEQ ID NO: 18 and two heavy chains each having the amino acid sequence of SEQ ID NO:19, wherein said treating is completely clearing palmoplantar psoriasis, the dosing regimen comprising:

a) subcutaneously administering to the patient a first dose of 150 mg of said anti-IL-23A antibody regardless of the patient's body weight; and

b) subcutaneously administering to the patient a second dose of 150 mg of said anti-IL-23A antibody regardless of the patient's body weight 4 weeks after said first dose is administered,

wherein the method results in the patient achieving complete clearance of palmoplantar psoriasis as measured by Palmoplantar Psoriasis Area Severity Index (PPASI) 2 weeks after receiving the first dose.

62. The method according to claim 61 , wherein beginning 12 weeks after the second dose is administered to the patient, a dose of 150 mg of the anti-IL-23A antibody is subcutaneously administered to the patient regardless of the patient's body weight once every 12 weeks.

63. A method for treating palmoplantar psoriasis, comprising administering to a human patient with palmoplantar psoriasis a therapeutically effective dosing regimen of a full-length anti-IL-23A antibody, said anti-IL-23A antibody comprising two light chains each having the amino acid sequence of SEQ ID NO: 18 and two heavy chains each having the amino acid sequence of SEQ ID NO:19, wherein said treating is completely clearing palmoplantar psoriasis, the dosing regimen comprising:

a) subcutaneously administering to the patient a first dose of 90 mg to 180 mg of said anti-IL-23A antibody regardless of the patient's body weight; and

b) subcutaneously administering to the patient a second dose of said anti-IL-23A antibody 4 weeks after said first dose is administered,

wherein the method results in the patient achieving complete clearance of palmoplantar psoriasis as measured by Palmoplantar Psoriasis Area Severity Index (PPASI) 2 weeks after receiving the first dose.

64. The method according to claim 63 , wherein beginning 12 weeks after the second dose is administered to the patient, additional doses of the anti-IL-23A antibody are subcutaneously administered to the patient once every 12 weeks and wherein said additional doses each comprise an amount of the anti-IL-23A antibody equal to the first dose regardless of the patient's body weight.

65. A method for treating nail psoriasis, comprising administering to a human patient with nail psoriasis a therapeutically effective dosing regimen of a full-length anti-IL-23A antibody, said anti-IL-23A antibody comprising two light chains each having the amino acid sequence of SEQ ID NO:18 and two heavy chains each having the amino acid sequence of SEQ ID NO: 19, wherein said treating is significantly reducing the severity of nail psoriasis, the dosing regimen comprising:

a) subcutaneously administering to the patient a first dose of 150 mg of said anti-IL-23A antibody regardless of the patient's body weight; and

b) subcutaneously administering to the patient a second dose of 150 mg of said anti-IL-23A antibody regardless of the patient's body weight 4 weeks after said first dose is administered,

wherein the method results in the patient achieving an improvement from baseline Nail Psoriasis Severity Index (NAPSI) 12 weeks after receiving the first dose.

66. The method according to claim 65 , wherein beginning 12 weeks after the second dose is administered to the patient, a dose of 150 mg of the anti-IL-23A antibody is subcutaneously administered to the patient regardless of the patient's body weight once every 12 weeks.

67. A method for treating nail psoriasis, comprising administering to a human patient with nail psoriasis a therapeutically effective dosing regimen of a full-length anti-IL-23A antibody, said anti-IL-23A antibody comprising two light chains each having the amino acid sequence of SEQ ID NO:18 and two heavy chains each having the amino acid sequence of SEQ ID NO: 19, wherein said treating is significantly reducing the severity of nail psoriasis, the dosing regimen comprising:

a) subcutaneously administering to the patient a first dose of 90 mg to 180 mg of said anti-IL-23A antibody regardless of the patient's body weight; and

b) subcutaneously administering to the patient a second dose of said anti-IL-23A antibody 4 weeks after said first dose is administered,

wherein the method results in the patient achieving an improvement from baseline Nail Psoriasis Severity Index (NAPSI) 12 weeks after receiving the first dose.

68. The method according to claim 67 , wherein beginning 12 weeks after the second dose is administered to the patient, additional doses of the anti-IL-23A antibody are subcutaneously administered to the patient once every 12 weeks and wherein said additional doses each comprise an amount of the anti-IL-23A antibody equal to the first dose regardless of the patient's body weight.

69. A method of treating scalp psoriasis, comprising administering to a human patient with scalp psoriasis a therapeutically effective dosing regimen of a full-length anti-IL-23A antibody, said anti-IL-23A antibody comprising two light chains each having the amino acid sequence of SEQ ID NO:18 and two heavy chains each having the amino acid sequence of SEQ ID NO: 19, wherein said treating is completely clearing scalp psoriasis, the dosing regimen comprising:

a) subcutaneously administering to the patient a first dose of 150 mg of said anti-IL-23A antibody regardless of the patient's body weight; and

b) subcutaneously administering to the patient a second dose of 150 mg of said anti-IL-23A antibody regardless of the patient's body weight 4 weeks after said first dose is administered,

wherein the method results in the patient achieving complete clearance of scalp psoriasis as measured by Psoriasis Scalp Severity Index (PSSI) 2 weeks after receiving the first dose.

70. The method according to claim 69 , wherein beginning 12 weeks after the second dose is administered to the patient, a dose of 150 mg of the anti-IL-23A antibody is subcutaneously administered to the patient regardless of the patient's body weight once every 12 weeks.

71. A method for treating scalp psoriasis, comprising administering to a human patient with scalp psoriasis a therapeutically effective dosing regimen of a full-length anti-IL-23A antibody, said anti-IL-23A antibody comprising two light chains each having the amino acid sequence of SEQ ID NO: 18 and two heavy chains each having the amino acid sequence of SEQ ID NO: 19, wherein said treating is completely clearing scalp psoriasis, the dosing regimen comprising:

a) subcutaneously administering to the patient a first dose of 90 mg to 180 mg of said anti-IL-23A antibody regardless of the patient's body weight; and

b) subcutaneously administering to the patient a second dose of said anti-IL-23A antibody 4 weeks after said first dose is administered,

wherein the method results in the patient achieving complete clearance of scalp psoriasis as measured by Psoriasis Scalp Severity Index (PSSI) 2 weeks after receiving the first dose.

72. The method according to claim 71 , wherein beginning 12 weeks after the second dose is administered to the patient, additional doses of the anti-IL-23A antibody are subcutaneously administered to the patient once every 12 weeks and wherein said additional doses each comprise an amount of the anti-IL-23A antibody equal to the first dose regardless of the patient's body weight.

73. A method of treating psoriatic arthritis, comprising administering to a human patient with psoriatic arthritis a therapeutically effective dosing regimen of a full-length anti-IL-23A antibody, said anti-IL-23A antibody comprising two light chains each having the amino acid sequence of SEQ ID NO:18 and two heavy chains each having the amino acid sequence of SEQ ID NO: 19, wherein said treating is improving one or more measures of psoriatic arthritis disease activity, the dosing regimen comprising:

a) subcutaneously administering to the patient a first dose of 150 mg of said anti-IL-23A antibody regardless of the patient's body weight; and

b) subcutaneously administering to the patient a second dose of 150 mg of said anti-IL-23A antibody regardless of the patient's body weight 4 weeks after said first dose is administered,

wherein the method results in the patient achieving at least a 50% reduction from baseline in pain as assessed by Visual Analogue Scale (pain-VAS) score at 12 weeks after receiving the first dose or the method results in the patient achieving at least a 90% reduction from baseline Psoriasis Area and Severity Index score (PASI 90) at 12 weeks after receiving the first dose.

74. The method according to claim 73 , wherein the method results in the patient achieving at least a 50% reduction from baseline in pain as assessed by Visual Analogue Scale (pain-VAS) score at 12 weeks after receiving the first dose.

75. The method according to claim 73 , wherein the method results in the patient achieving at least a 90% reduction from baseline Psoriasis Area and Severity Index score (PASI 90) at 12 weeks after receiving the first dose.

76. The method according to claim 73 , wherein beginning 12 weeks after the second dose is administered to the patient, a dose of 150 mg of the anti-IL-23A antibody is subcutaneously administered to the patient regardless of the patient's body weight once every 12 weeks.

77. A method for treating psoriatic arthritis, comprising administering to a human patient with psoriatic arthritis a therapeutically effective dosing regimen of a full-length anti-IL-23A antibody, said anti-IL-23A antibody comprising two light chains each having the amino acid sequence of SEQ ID NO:18 and two heavy chains each having the amino acid sequence of SEQ ID NO: 19, wherein said treating is improving one or more measures of psoriatic arthritis disease activity, the dosing regimen comprising:

a) subcutaneously administering to the patient a first dose of 90 mg to 180 mg of said anti-IL-23A antibody regardless of the patient's body weight; and

b) subcutaneously administering to the patient a second dose of said anti-IL-23A antibody 4 weeks after said first dose is administered,

wherein the method results in the patient achieving at least a 50% reduction from baseline in pain as assessed by Visual Analogue Scale (pain-VAS) score at 12 weeks after receiving the first dose or the method results in the patient achieving at least a 90% reduction from baseline Psoriasis Area and Severity Index score (PASI 90) at 12 weeks after receiving the first dose.

78. The method according to claim 77 , wherein the method results in the patient achieving at least a 50% reduction from baseline in pain as assessed by Visual Analogue Scale (pain-VAS) score at 12 weeks after receiving the first dose.

79. The method according to claim 77 , wherein the method results in the patient achieving at least a 90% reduction from baseline Psoriasis Area and Severity Index score (PASI 90) at 12 weeks after receiving the first dose.

80. The method according to claim 77 , wherein beginning 12 weeks after the second dose is administered to the patient, additional doses of the anti-IL-23A antibody are subcutaneously administered to the patient once every 12 weeks and wherein said additional doses each comprise an amount of the anti-IL-23A antibody equal to the first dose regardless of the patient's body weight.

Assignments (1)
ASSIGNMENT OF ASSIGNOR'S INTEREST Recorded Apr 12, 2017
From: ARNDT, MATTHIAS; ASLANYAN, STELLA; FLACK, MARY RUTH; GALLER, ANNETTE BETTINA; LALOVIC, BOJAN; PADULA, STEVEN JOHN; SCHOLL, PAUL
To: BOEHRINGER INGELHEIM INTERNATIONAL GMBH
Reel/Frame 041978/0001 →
Continuity (7)
Provisional Application 62235631 · Oct 1, 2015
Provisional Application 62204520 · Aug 13, 2015
Provisional Application 62145764 · Apr 10, 2015
Provisional Application 62135335 · Mar 19, 2015
Provisional Application 62130876 · Mar 10, 2015
Provisional Application 62111731 · Feb 4, 2015
Related Publication 20160222102A1 · Aug 4, 2016
References Cited (400)
US 4179337A · Davis et al. · 1979 [cited by applicant]
US 4275149A · Litman et al. · 1981 [cited by applicant]
US 4301144A · Iwashita et al. · 1981 [cited by applicant]
US 4318980A · Boguslaski et al. · 1982 [cited by applicant]
US 4419446A · Howley et al. · 1983 [cited by applicant]
US 4485045A · Rogen · 1984 [cited by applicant]
US 4496689A · Mitra · 1985 [cited by applicant]
US 4544545A · Ryan et al. · 1985 [cited by applicant]
US 4560655A · Baker · 1985 [cited by applicant]
US 4601978A · Karin · 1986 [cited by applicant]
US 4640835A · Shimizu et al. · 1987 [cited by applicant]
US 4657866A · Kumar · 1987 [cited by applicant]
US 4670417A · Iwasaki et al. · 1987 [cited by applicant]
US 4737456A · Weng et al. · 1988 [cited by applicant]
US 4741900A · Alvarez et al. · 1988 [cited by applicant]
US 4767704A · Cleveland et al. · 1988 [cited by applicant]
US 4791192A · Nakagawa et al. · 1988 [cited by applicant]
US 4816567A · Cabilly et al. · 1989 [cited by applicant]
US 4927762A · Darfler · 1990 [cited by applicant]
US 4965199A · Capon et al. · 1990 [cited by applicant]
US 4975278A · Senter et al. · 1990 [cited by applicant]
US 5013556A · Woodle et al. · 1991 [cited by applicant]
US 5122469A · Mather et al. · 1992 [cited by applicant]
US 5888809A · Allison · 1999 [cited by applicant]
US 6037454A · Jardieu et al. · 2000 [cited by applicant]
US 6054297A · Carter et al. · 2000 [cited by applicant]
US 6060284A · Bazan · 2000 [cited by applicant]
US 6407213B1 · Carter et al. · 2002 [cited by applicant]
US 6479634B1 · Bazan · 2002 [cited by applicant]
US 6495667B1 · Bazan · 2002 [cited by applicant]
US 6610285B1 · Hirata · 2003 [cited by applicant]
US 6756481B2 · Chirica et al. · 2004 [cited by applicant]
US 6835825B1 · Bazan · 2004 [cited by applicant]
US 7090847B1 · Oppmann et al. · 2006 [cited by applicant]
US 7183382B2 · Oppmann et al. · 2007 [cited by applicant]
US 7252967B2 · Hirata · 2007 [cited by applicant]
US 7282204B2 · Oft et al. · 2007 [cited by applicant]
US 7332156B2 · Bowman et al. · 2008 [cited by applicant]
US 7411041B2 · Chirica et al. · 2008 [cited by applicant]
US 7422743B2 · Chirica et al. · 2008 [cited by applicant]
US 7427402B2 · Kastelein et al. · 2008 [cited by applicant]
US 7491391B2 · Benson et al. · 2009 [cited by applicant]
US 7501247B2 · Kastelein et al. · 2009 [cited by applicant]
US 7510709B2 · Gurney · 2009 [cited by applicant]
US 7510853B2 · Chirica et al. · 2009 [cited by applicant]
US 7575741B2 · Bowman et al. · 2009 [cited by applicant]
US 7608690B2 · Bazan · 2009 [cited by applicant]
US 7740848B2 · Kastelein et al. · 2010 [cited by applicant]
US 7749718B2 · Chirica et al. · 2010 [cited by applicant]
US 7750126B2 · Hirata · 2010 [cited by applicant]
US 7754214B2 · Chirica et al. · 2010 [cited by applicant]
US 7790862B2 · Lewis et al. · 2010 [cited by applicant]
US 7807160B2 · Presta et al. · 2010 [cited by applicant]
US 7807414B2 · Benson et al. · 2010 [cited by applicant]
US 7820168B2 · Cua et al. · 2010 [cited by applicant]
US 7872102B2 · Beidler et al. · 2011 [cited by applicant]
US 7883695B2 · Oppmann et al. · 2011 [cited by applicant]
US 7887806B2 · Chirica et al. · 2011 [cited by applicant]
US 7893215B2 · Bowman et al. · 2011 [cited by applicant]
US 7910703B2 · Lewis et al. · 2011 [cited by applicant]
US 7935344B2 · Benson et al. · 2011 [cited by applicant]
US 7993645B2 · Benson et al. · 2011 [cited by applicant]
US 8106177B2 · Benson et al. · 2012 [cited by applicant]
US 8778346B2 · Barrett et al. · 2014 [cited by applicant]
US 9441036B2 · Barrett et al. · 2016 [cited by applicant]
US 10202448B2 · Barrett et al. · 2019 [cited by applicant]
US 10507241B2 · Visvanathan et al. · 2019 [cited by applicant]
US 11078265B2 · Nabozny et al. · 2021 [cited by applicant]
US 11572385B2 · Garidel et al. · 2023 [cited by applicant]
US 20040219150A1 · Cua et al. · 2004 [cited by applicant]
US 20040258686A1 · Chirica et al. · 2004 [cited by applicant]
US 20050039222A1 · Habu et al. · 2005 [cited by applicant]
US 20050100917A1 · Chirica et al. · 2005 [cited by applicant]
US 20050100918A1 · Chirica et al. · 2005 [cited by applicant]
US 20050100965A1 · Ghayur et al. · 2005 [cited by applicant]
US 20050208052A1 · Katsikis et al. · 2005 [cited by applicant]
US 20050244874A1 · Kastelein et al. · 2005 [cited by applicant]
US 20050287593A1 · Kastelein et al. · 2005 [cited by applicant]
US 20060088523A1 · Andya et al. · 2006 [cited by applicant]
US 20060140958A1 · Hogan et al. · 2006 [cited by applicant]
US 20070009526A1 · Benson et al. · 2007 [cited by applicant]
US 20070218060A1 · Long et al. · 2007 [cited by applicant]
US 20080199460A1 · Cua et al. · 2008 [cited by applicant]
US 20080200655A1 · Sek · 2008 [cited by applicant]
US 20080254026A1 · Long et al. · 2008 [cited by applicant]
US 20080311043A1 · Hoffman et al. · 2008 [cited by applicant]
US 20090060906A1 · Barry et al. · 2009 [cited by applicant]
US 20090092604A1 · Cua et al. · 2009 [cited by applicant]
US 20090123479A1 · Bembridge et al. · 2009 [cited by applicant]
US 20090156788A1 · Presta et al. · 2009 [cited by applicant]
US 20090291062A1 · Fraunhofer et al. · 2009 [cited by applicant]
US 20100003251A1 · Oft et al. · 2010 [cited by applicant]
US 20100041144A1 · Bazan · 2010 [cited by applicant]
US 20100111950A1 · Cua et al. · 2010 [cited by applicant]
US 20100111954A1 · Cua et al. · 2010 [cited by applicant]
US 20100111966A1 · Presta et al. · 2010 [cited by applicant]
US 20100135998A1 · Bowman et al. · 2010 [cited by applicant]
US 20100143357A1 · Cua et al. · 2010 [cited by applicant]
US 20100172862A1 · Correia et al. · 2010 [cited by applicant]
US 20100254991A1 · Kastelein et al. · 2010 [cited by applicant]
US 20100261273A1 · Chirica et al. · 2010 [cited by applicant]
US 20100266582A1 · Gurney · 2010 [cited by applicant]
US 20100266583A1 · Gurney · 2010 [cited by applicant]
US 20100272731A1 · Presta et al. · 2010 [cited by applicant]
US 20100291084A1 · Kopf et al. · 2010 [cited by applicant]
US 20100322863A1 · Benson et al. · 2010 [cited by applicant]
US 20110002942A1 · Presta et al. · 2011 [cited by applicant]
US 20110059087A1 · Lewis et al. · 2011 [cited by applicant]
US 20110135597A1 · Bowman et al. · 2011 [cited by applicant]
US 20110142831A1 · Cua et al. · 2011 [cited by applicant]
US 20110142853A1 · Presta et al. · 2011 [cited by applicant]
US 20110159589A1 · Lewis et al. · 2011 [cited by applicant]
US 20110177022A1 · Oppmann et al. · 2011 [cited by applicant]
US 20110195455A1 · Benson et al. · 2011 [cited by applicant]
US 20110206686A1 · Bembridge et al. · 2011 [cited by applicant]
US 20110212104A1 · Beaumont et al. · 2011 [cited by applicant]
US 20110229490A1 · Li et al. · 2011 [cited by applicant]
US 20110250201A1 · Smith · 2011 [cited by applicant]
US 20110311527A1 · Stern et al. · 2011 [cited by applicant]
US 20120128689A1 · Clarkson et al. · 2012 [cited by applicant]
US 20120195885A1 · Correia et al. · 2012 [cited by applicant]
US 20120277799A1 · Winslow et al. · 2012 [cited by applicant]
US 20120282269A1 · Barrett et al. · 2012 [cited by applicant]
US 20130004501A1 · Towne et al. · 2013 [cited by applicant]
US 20130028907A1 · Parshad et al. · 2013 [cited by applicant]
US 20130115166A1 · Clarke et al. · 2013 [cited by applicant]
US 20130216525A1 · Chen · 2013 [cited by applicant]
US 20140046063A1 · Moussy et al. · 2014 [cited by applicant]
US 20140178401A1 · Nabozny et al. · 2014 [cited by applicant]
US 20140303357A1 · Lim et al. · 2014 [cited by applicant]
US 20140363444A1 · Barrett et al. · 2014 [cited by applicant]
US 20160060338A1 · Barrett et al. · 2016 [cited by applicant]
US 20160222102A1 · Arndt et al. · 2016 [cited by applicant]
US 20160304602A1 · Arndt et al. · 2016 [cited by applicant]
US 20160333091A1 · Barrett et al. · 2016 [cited by applicant]
US 20170022294A1 · Singh et al. · 2017 [cited by applicant]
US 20170081402A1 · Boecher et al. · 2017 [cited by applicant]
US 20170157246A1 · Visvanathan et al. · 2017 [cited by applicant]
US 20170298126A1 · Baum et al. · 2017 [cited by applicant]
US 20180009887A1 · Arndt-Schmitz et al. · 2018 [cited by applicant]
US 20180105588A1 · Baum et al. · 2018 [cited by applicant]
US 20180334501A1 · Arndt-Schmitz et al. · 2018 [cited by applicant]
US 20190309016A1 · Garidel et al. · 2019 [cited by applicant]
US 20200299378A1 · Baum et al. · 2020 [cited by applicant]
US 20200308271A1 · Baum et al. · 2020 [cited by applicant]
US 20200376117A1 · Visvanathan et al. · 2020 [cited by applicant]
US 20210070852A1 · Garidel et al. · 2021 [cited by applicant]
US 20210198355A1 · Barrett et al. · 2021 [cited by applicant]
US 20210317201A1 · Nabozny et al. · 2021 [cited by applicant]
DE DD266710A3 · 1989 [cited by applicant]
EP 073657A1 · 1983 [cited by applicant]
EP 0183070A2 · 1986 [cited by applicant]
EP 0244234A2 · 1987 [cited by applicant]
EP 0402226A1 · 1990 [cited by applicant]
EP 1072610A1 · 2001 [cited by applicant]
EP 2786746A1 · 2014 [cited by applicant]
JP 2015517465A · 2015 [cited by applicant]
WO WO8101145A1 · 1981 [cited by applicant]
WO WO8700195A1 · 1987 [cited by applicant]
WO WO8807378A1 · 1988 [cited by applicant]
WO WO9003430A1 · 1990 [cited by applicant]
WO WO9013646A1 · 1990 [cited by applicant]
WO WO9404188A1 · 1994 [cited by applicant]
WO WO9411026A2 · 1994 [cited by applicant]
WO WO9624369A1 · 1996 [cited by applicant]
WO WO9632478A1 · 1996 [cited by applicant]
WO WO9905280A1 · 1999 [cited by applicant]
WO WO9940195A1 · 1999 [cited by applicant]
WO WO9954357A1 · 1999 [cited by applicant]
WO WO011805A2 · 2001 [cited by applicant]
WO WO0185790A2 · 2001 [cited by applicant]
WO WO03039485A2 · 2003 [cited by applicant]
WO WO2004042009A2 · 2004 [cited by applicant]
WO WO2004058178A2 · 2004 [cited by applicant]
WO WO2004071517A2 · 2004 [cited by applicant]
WO WO2004081190A2 · 2004 [cited by applicant]
WO WO2005044294A2 · 2005 [cited by applicant]
WO WO2005052157A1 · 2005 [cited by applicant]
WO WO2005079837A1 · 2005 [cited by applicant]
WO WO2005108616A1 · 2005 [cited by applicant]
WO WO2006036922A2 · 2006 [cited by applicant]
WO WO2006068987A2 · 2006 [cited by applicant]
WO WO2007005647A2 · 2007 [cited by applicant]
WO WO2007005955A2 · 2007 [cited by applicant]
WO WO2007024846A2 · 2007 [cited by applicant]
WO WO2007027714A2 · 2007 [cited by applicant]
WO WO2007027761A2 · 2007 [cited by applicant]
WO WO2007076523A2 · 2007 [cited by applicant]
WO WO2007076524A2 · 2007 [cited by applicant]
WO WO2007147019A2 · 2007 [cited by applicant]
WO WO2007149814A1 · 2007 [cited by applicant]
WO WO2008101145A1 · 2008 [cited by applicant]
WO WO2008103432A1 · 2008 [cited by applicant]
WO WO2008103473A1 · 2008 [cited by applicant]
WO WO2008106131A2 · 2008 [cited by applicant]
WO WO2008153610A2 · 2008 [cited by applicant]
WO WO2009032954A1 · 2009 [cited by applicant]
WO WO2009043933A1 · 2009 [cited by applicant]
WO WO2009053493A1 · 2009 [cited by applicant]
WO WO2009055936A1 · 2009 [cited by applicant]
WO WO2009073569A2 · 2009 [cited by applicant]
WO WO2009082624A2 · 2009 [cited by applicant]
WO WO2010017598A1 · 2010 [cited by applicant]
WO WO2010027766A1 · 2010 [cited by applicant]
WO WO2010115092A2 · 2010 [cited by applicant]
WO WO2010115786A1 · 2010 [cited by applicant]
WO WO2011011797A2 · 2011 [cited by applicant]
WO WO2011056600A1 · 2011 [cited by applicant]
WO WO2011066369A2 · 2011 [cited by applicant]
WO WO2011070339A1 · 2011 [cited by applicant]
WO WO2011103105A1 · 2011 [cited by applicant]
WO WO2011104381A2 · 2011 [cited by applicant]
WO WO2011109365A2 · 2011 [cited by applicant]
WO WO2011159655A2 · 2011 [cited by applicant]
WO WO2011159750A1 · 2011 [cited by applicant]
WO WO2012009760A1 · 2012 [cited by applicant]
WO WO2012032181A2 · 2012 [cited by applicant]
WO WO2012061448A1 · 2012 [cited by examiner]
WO WO2012093254A1 · 2012 [cited by applicant]
WO WO2012103345A1 · 2012 [cited by applicant]
WO WO2013165791A1 · 2013 [cited by applicant]
WO WO2013186230A1 · 2013 [cited by applicant]
WO WO2014004436A2 · 2014 [cited by applicant]
WO WO2014143540 · 2014 [cited by applicant]
WO WO2014149425A1 · 2014 [cited by applicant]
WO WO2016014775A1 · 2016 [cited by applicant]
WO WO2016036918A1 · 2016 [cited by applicant]
WO WO2017048901A1 · 2017 [cited by applicant]
WO WO2018011404A1 · 2018 [cited by applicant]
WO WO2019246271A1 · 2019 [cited by applicant]
WO WO2024085697 · 2024 [cited by applicant]
Paul. Fundamental Immunology, 3rd Edition, Raven Press, New York, Chapter 8, pp. 292-295, 1993 (Year: 1993). [cited by examiner]
MacCallum et al. Antibody-antigen interactions: contact analysis and binding topography. Journal of Molecular Biology, 262:732-745, 1996 (Year: 1996). [cited by examiner]
Casset et al. A peptide mimetic of an anti-CD4 monoclonal antibody by rational design. Biochemical and Biophysical Research Communications, 307: 198-205, 2003. (Year: 2003). [cited by examiner]
Vajdos et al. Comprehensive Functional Maps of the Antigen binding Site of an Anti-ErbB2 Antibody Obtained with Shotgun Scanning Mutagenesis. Journal of Molecular Biology, Jul. 5, 2002; 320(2):415-28 (Year: 2002). [cited by examiner]
Kim et al. Diagnosis and management of psoriasis. Canadian Family Physician, 2017;63:278-85 (Year: 2017). [cited by examiner]
Alunno et al. Targeting the IL-23/IL-17 axis for the treatment of psoriasis and psoriatic arthritis. Expert Opinion on Biological Therapy, 2015;15:12, 1727-1737 (Year: 2015). [cited by examiner]
Campa et al. A review of biologic therapies targeting IL-23 and IL-17 for use in moderate-to-severer plaque psoriasis. Dermatology Therapy, 2016; 6:1-12 (Year: 2016). [cited by examiner]
ClinicalTrials.gov study NCT01018810, published Nov. 24, 2009 (downloaded from https://clinicaltrials.gov/ct2/history/NCT01018810) (Year: 2009). [cited by examiner]
ClinicalTrials.gov study NCT01483599, published Nov. 29, 2011 (downloaded fromhttps://clinicaltrials.gov/ct2/history/NCT01483599) (Year: 2011). [cited by examiner]
ClinicalTrials.gov study NCT02319759, published Dec. 15, 2014 (downloaded fromhttps://clinicaltrials.gov/ct2/history/NCT02319759) (Year: 2014). [cited by examiner]
ClinicalTrials.gov study NCT01729754, published Nov. 14, 2012 (downloaded fromhttps://clinicaltrials.gov/ct2/history/NCT01729754) (Year: 2012). [cited by examiner]
ClinicalTrials.gov study NCT01483599, published Nov. 29, 2011 (downloaded fromhttps://clinicaltrials.gov/ct2/history/ NCT01483599) (Year: 2011). [cited by examiner]
ClinicalTrials.gov study NCT02319759, published Dec. 15, 2014 (downloaded fromhttps://clinicaltrials.gov/ct2/history/ NCT02319759) (Year: 2014). [cited by examiner]
ClinicalTrials.gov study NCT01729754, published Nov. 14, 2012 (downloaded fromhttps://clinicaltrials.gov/ct2/history/ NCT01729754) (Year: 2012). [cited by examiner]
Aggarwal et al., “Interleukin-23 Promotes a Distinct CD4 T Cell Activation State Characterized by the Production of Interleukin-17,” Journal of Biological Chemistry, 2003, 278(3): 1910-1914. [cited by applicant]
Alegre et al., “A Non-Activativing “Humanized” Anti-CD3 Monoclonal Antibody Retains Immunosuppressive Properties in Vivo,” Transplantation; Jun. 1994, 57(11):1537-1543. [cited by applicant]
Anonymous: “A 52-Week, Phase 3, Randomized, Active Comparator and Placebo-Controlled, Parallel Design Study to Evaluate the Efficacy and Safety/Tolerability of Subcutaneous SCH 9000222/MK-3222, Followed by an Optional L… [cited by applicant]
Anonymous: “A Phase 2 Multicenter, Randomized, Pacebo- and Active-Comparator-Controlled, Dose-Ranging Trial to Evaluate CNTO 1959 for the Treatment of Subjects with Moderate to Sever Plaque-type Psoriasis (X-PLORE)” Mar… [cited by applicant]
Anonymous: “A Phase 2a, Multicenter, Randomized, Double-blind, Placebo-controlled Study Evaluating the Efficacy and Safety of Guselkumab in the Treatment of Subjects with Active Psoriatic Arthritis,” Jan. 26, 2015, 4 pa… [cited by applicant]
Baerveldt et al., “Ustekinumab improves psoriasis-related gene expression in noninvolved psoriatic skin without inhibition of the antimicrobial response,” British Journal of Dermatology, 2013, 168:990-998. [cited by applicant]
Beyer et al., “Crystal Structures of the Pro-Inflammatory Cytokine Interleukin-23 and its Complex with a High-Affinity Neutralizing Antibody,” Journal of Molecular Biology, 2008, 382:942-955. [cited by applicant]
Bhambhani et al., “Formulation Design and High-Throughput Excipient Selection Based on Structural Integrity and Conformational Stability of Dilute and Highly Concentrated IgG1 Monoclonal Antibody Solutions,” Journal of … [cited by applicant]
Brodmerkel et al., “The Skin and Circulating Immune Profile of Therapeutic IL-12/23 Blockade in Psoriasis Patients Treated with Ustekinumab,” Clinical Immunology, Academic Press, Jan. 1, 2009, 131:S5, Abstract. [cited by applicant]
Cao et al., “Anti-IL-23 antibody blockade of IL-23/IL-17 pathway attenuates airway obliteration in rat orthotopic tracheal transplantation,” International Immunopharmacology, 2011, 11:569-575. [cited by applicant]
Castro et al., “Reslizumab for Poorly Controlled, Eosinophilic Asthma, A Randomized, Placebo-controlled Study,” Am. J. Respir. Crit. Care Med., 2011, 184:1125-1132. [cited by applicant]
Catalog No. AF1716. “Anti-human IL-23 p19 Antibody,” Lot No. JMB01., R&D Systems, Inc., Dec. 17, 2003. [cited by applicant]
Chan et al., “Therapeutic antibodies for autoimmunity and inflammation,” Nature Reviews, Immunology, May 2010, 10:301-316. [cited by applicant]
Choy et al., “Th2 and Th17 inflammatory pathways are reciprocally regulated in asthma,” www.ScienceTranslationalMedicine.org, 2015, 7(301):301 ra129, 11 pages. [cited by applicant]
Ciprandi et al., “Serum IL-23 Strongly and Inversely Correlates with FEV1 in Asthmatic Children,” International Archives of Allergy and Immunology, 2012, 159(2):183-186. [cited by applicant]
Croxford et al., IL-12 and IL-23 in health and disease,: Cytokine & Growth Factor Reviews, 2014, 25:415-421. [cited by applicant]
Cupparic et al., “Serum IL-23 in Asthmatic Children,” Journal of Biological Regulators & Homeostatic Agents, 2012, 26(1(S)):53-61. [cited by applicant]
Daugherty et al., “Formulation and delivery issues for monoclonal antibody therapeutics,” Advanced Drug Delivery Reviews, 2006, 58:686-706. [cited by applicant]
eBioscience, Anti-Mouse IL-23 p 19 Purified; Catalog No. 14-7232; Clone G23-8; According to all information that could be obtained from publicly available sources by Applicants, G23-8 antibody was available for purchase… [cited by applicant]
eBioscience, Anti-Mouse IL-23 p 19 Purified; Catalog No. 14-7233; Clone 5B2; According to all information that could be obtained from publicly available sources by Applicants, 5B2 antibody was available for purchase in … [cited by applicant]
eBioscience, Mouse IL-23 ELISA Ready-Set-Go! ELISA Kit, Catalog No. 88-7923, 6 pages. According to all information that could be obtained from publicly available sources by Applicants, Mouse IL-23 ELISA Ready-Set-Go! EL… [cited by applicant]
Eijnden, Serge Vanden et al., “Preferential production of the IL-12(p40)/IL-23(19) heterodimer by dendritic cells from human newborns,” Eur. J. Immunol., 2006, 36:21-26. [cited by applicant]
Fahy, John V., “Eosinophilic and Neutrophilic Inflammation in Asthma, Insights from Clinical Studies,” Proceedings of the American Thoracic Society, 2009, 6:256-259. [cited by applicant]
Fichtner-Feigl et al., “Treatment of murine Th1- and Th2-mediated inflammatory bowel disease with NF-κB decoy oligonucleotides,” Journal of Clinical Investigation, Nov. 2005, 115(11):3057-3071. [cited by applicant]
Gaffen et al., “The IL-23-1L-17 immune axis: from mechanisms to therapeutic testing,” Nature Reviews, 2014, 14:585-600. [cited by applicant]
Gordon et al., “A Phase 2 Trial of Guselkumab versus Adalimumab for Plaque Psoriasis,” New England Journal of Medicine, 2015, 373(2):136-144. [cited by applicant]
Gudjonsson et al., “Assessment of the Psoriatic Transcriptome in a Large Sample: Additional Regulated Genes and Comparisons with in Vitro Models,” Journal of Investigative Dermatology, 2010, 130:1829-1840. [cited by applicant]
Haldar et al., “Mepolizumab and Exacerbations of Refractory Eosinophilic Asthma,” The New England Journal of Medicine, 2009, 360:973-984. [cited by applicant]
Happel et al., “Divergent roles of IL-23 and IL-12 in host defense against Klebsiella pneumoniae” Journal of Experimental Medicine, Sep. 2005, 202(6):761-769. [cited by applicant]
Hegazi et al., “Carbon monoxide ameliorates chronic murine colitis through a heme oxygenase 1-dependent pathway,” Journal of Experimental Medicine, Dec. 2005, vol. 202, No. 12, pp. 1703-1713. [cited by applicant]
Hegyi et al., “Vitamin D Analog Calcipotriol Suppresses the Th17 Cytokine-Induced Proinflammatory S100 ‘Alarmins’ Psoriasin (S100A7) and Koebnerisin (S100A15) in Psoriasis,” Journal of Investigative Dermatology, 2012, 1… [cited by applicant]
Hoeve et al., “IL-12 receptor deficiency revisited: IL-23-mediated signaling is also impaired in human genetic IL-12 receptor ?1deficiency,” Eur. J. Immunol., 2003, 33:3393-3397. [cited by applicant]
Hu et al., “Information contributed by meta-analysis in exposure-response modeling: application to phase 2 does selection of guselkumab in patients with moderate-to-severe psoriasis,” Journal of Pharmacokinet. Pharmacod… [cited by applicant]
International Preliminary Report on Patentability and Written Opinion for PCT/US2015/041706 dated Feb. 2, 2017. [cited by applicant]
International Preliminary Report on Patentability for PCT/US2011/058869 dated May 7, 2013. [cited by applicant]
International Search Report & Written Opinion for PCT/US2011/058869, dated Feb 27, 2012. [cited by applicant]
International Search Report and Written Opinion dated Jul. 28, 2017, in PCT/US2017/027332. [cited by applicant]
International Search Report and Written Opinion dated Oct. 26, 2017 in PCT/US2016/027263. [cited by applicant]
International Search Report for PCT/US2013/038109 dated Apr. 25, 2013. [cited by applicant]
International Search Report for PCT/US2015/041706 dated Oct. 15, 2015. [cited by applicant]
International Search Report for PCT/US2016/016061 dated May 18, 2016. [cited by applicant]
International Search Report for PCT/US2016/027263 dated Jun. 29, 2016. [cited by applicant]
International Search Report for PCT/US2016/051844 dated Jan. 10, 2017. [cited by applicant]
Irvin et al., “Increased frequency of dual-positive TH2/TH17 cells in bronchoalveolar lavage fluid characterizes a population of patients with severe asthma,” Journal of Allergy and Clinical Immunology, 2014, 134(5):117… [cited by applicant]
Kastelein et al., “Discovery and Biology of IL-23 and IL-27: Related but Functionally Distinct Regulators of Inflammation,” Annual Reviews Immunology, 2007, 25: 221-242. [cited by applicant]
Kerdel et al., “An evolution in switching therapy for psoriasis patients who fail to meet treatment goals,” Dermatologic Therapy, 2015, 28:390-403. [cited by applicant]
Kidoya et al., “Fas Ligand Induces Cell-Autonomous IL-23 Production in Dendritic Cells, a Mechanism for Fas Ligand-Induced IL-17 Production,” Journal of Immunology, 2005, 8024-8031. [cited by applicant]
Kikly et al., “The IL-23/Th17 axis: Therapeutic targets for autoimmune inflammation,” Current Opinion in Immunology, 2006, 18:670-675. [cited by applicant]
Kofoed et al “New Drugs and Treatment Targets in Psoriasis,” Acta Derm. Venereol., 2015, 95:133-139. [cited by applicant]
Kopp et al., “Clinical improvement in psoriasis with specific targeting of interleukin-23,” Nature, 2015, 521(7551):222-226. [cited by applicant]
Krishnan et al., “Development of Formulations for Therapeutic Monoclonal Antibodies and Fc Fusion Proteins,” Formulation and Process Development Strategies for Manufacturing Biopharmaceuticals, 2010, Chapter 16, 383-427. [cited by applicant]
Kuwashima et al., “Delivery of Dendritic Cells Engineered to Secrete IFN-? into Central Nervous System Tumors Enhances the Efficacy of Peripheral Tumor Cell Vaccines: Dependence on Apoptotic Pathways,” Journal of Immuno… [cited by applicant]
Langowski et al,. “IL-23 promotes tumour incidence and growth,” Nature, Jul. 2006, 442(27):461-465. [cited by applicant]
Lee et al., “Increased Expression of Interleukin 23 p19 and p40 in Lesional Skin of Patients with Psoriasis Vulgaris,” Journal of Experimental Medicine, 2004, 199(1):125-130. [cited by applicant]
Leonardi et al., “Efficacy and safety of ustekinumab, a human interleukin-12/23 monoclonal antibody, in patients with psoriasis: 76-weeks results form a randomised, double-blind, placebo-controlled trail (PHOENIX 1),” T… [cited by applicant]
Li et al., “Silencing IL-23 expression by a small hairpin RNA protects against asthma in mice,” Experimental and Molecular Medicine, 2011, 43(4):197-204. [cited by applicant]
Mallbris et al., “Neutrophil gelatinase-associated lipocalin is a marker for dysregulated keratinocyte differentiation in human skin” Experimental Dermatology, 2002, 11:584-591. [cited by applicant]
McInnes et al., “Efficacy and safety of secukinumab, a fully human anti-interleukin-17A monoclonal antibody, in patients with moderate-to-severe psoriatic arthritis: a 24-week, randomised, double-blind, placebo-controll… [cited by applicant]
McKinley et al., “TH17 Cells Mediate Steroid-Resistant Airway Inflammation and Airway Hyperresponsiveness in Mice,” The Journal of Immunology, 2008, 181:4089-4097. [cited by applicant]
Morelli et al., “CD4+ T Cell Responses Elicted by Different Subsets of Human Skin Migratory Dendritic Cells,” The Journal of Immunology, 2005, 175:7905-7915. [cited by applicant]
Naji et al., “T Helper 17 Cells and Related Cytokines after Allergen Inhalation Challenge in Allergic Asthmatics,” International Archives of Allergy & Immunology, 2014, 165:27-34. [cited by applicant]
Nakajima et al., “Role of IL-23 and Th17 Cells in Airway Inflammation in Asthma,” Immune Network, 2010, 10(1):1-4. [cited by applicant]
Narasimhan et al., “High-dose monoclonal antibodies via the subcutaneous route: challenges and technical solutions, an industry perspective,” Therapeutic Delivery, 2012, 3(7):889-900. [cited by applicant]
Oppmann et al., Novel p19 Protein Engages IL-12p40 to Form a Cytokine, IL-23, with Biological Activities Similar as Well as Distinct from IL-12,$201D Immunity, 2000, 13:715-725. [cited by applicant]
Papp et al., “Tildrakizumab (MK-3222) an anti-interleukin-23p19 monoclonal antibody, improves psoriasis in a phase Ilb randomized placebo-controlled trial,” British Journal of Dermatology, 2015, 173:930-939. [cited by applicant]
Parham et al., “A Receptor for the Heterodimeric Cytokine IL-23 is Composed of IL-12Rß1 and a Novel Cytokine Receptor Subunit, IL-23R,” Journal of Immunology, 2002, 168:5699-5708. [cited by applicant]
Patel et al., “Emerging Therapies for the Treatment of Psoriasis” Dermatol Ther. (Heidelb), 2012, 2:16, 10 pages. [cited by applicant]
Pirhonen et al., “Regulation of Virus-Induced IL-12 and IL-23 Expression in Human Macrophages,” Journal of Immunology, 2002, 5673-5678. [cited by applicant]
Piskin et al., “Clinical Improvement in chronic plaque-type psoriasis lesions after narrow-band UVB therapy is accompanied by a decrease in the expression of IFN-y inducers—IL-12, IL-18, and IL-23,” Experimental Dermato… [cited by applicant]
Piskin, Gamze “IL-23 Expression by Keratinocytes,” Effects of Therapies on Cytokine Patterns of Psoriasis, 2004, Chapter 7, 114-131. [cited by applicant]
R&D Systems New Products, Jun. 2005. 12 pgs. www.RnDSystems.com. [cited by applicant]
R&D Systems, de novo newsletter, Mar. 2004, 10 pgs. www.rndsystems.com. [cited by applicant]
Rouet et al., “Stability engineering of the human antibody repertoire,” FEBS Letters, 2014, 588:269-277. [cited by applicant]
Savage et al. “Ustekinumab in the Treatment of Psoriasis and Psoriatic Arthritis,” Rheumatol. Ther., 2015, 2:1-16. [cited by applicant]
Sehy et al., Abstract 560.34 “Unambiguous Detection of IL-23 (p19/p40) Protein in Native Samples Using a Novel Enzyme-Linked Immunosorbent Assay,” Experimental Biology, 2005, A945-A946, International Congress of Physiol… [cited by applicant]
Shire, Steven J., Monoclonal Antibodies: Meeting the Challenges in Manufacturing, Formulation, Delivery and Stability of Final Drug Product, 2015. [cited by applicant]
Singh et al., “Selective targeting of the IL23 pathway: Generation and characterization of a novel high-affinity humanized anti-IL23A antibody,” MABS, Apr. 23, 2015, 7(4):778-791. [cited by applicant]
Sofen et al., “Guselkumab (an IL-23-specific mAb) demonstrates clinical and molecular response in patients iwth moderate-to-severe psoriasis,” Journal of Allergy and Clinical Immunology, 2014,133:1032-1040. [cited by applicant]
Suarez-Farinas et al., “Expanding the Psoriasis Disease Profile: Interrogation of the Skin and Serum of Patients with Moderate-to-Severe Psoriasis,” Journal of Investigative Dermatology, 2012, 132:2552-2564. [cited by applicant]
Tang et al., “Interleukin-23: as a drug target for autoimmune inflammatory diseases,” Immunology, 2011, 135:112-124. [cited by applicant]
Tian et al., “Meta-Analysis Derived (MAD) Transcriptome of Psoriasis Defines the “Core” Patheogenesis of Disease,” PLOS One, 2012, 7(9):e44274, 15 pages. [cited by applicant]
U.S. Office Action on U.S. Appl. No. 13/870,061 dated Mar. 9, 2018. [cited by applicant]
U.S. Appl. No. 13/870,061, filed Apr. 25, 2013. First named inventor: Gerald Henry Nabozny. [cited by applicant]
U.S. Appl. No. 14/302,986, filed Jun. 12, 2014. First named inventor: Rachel Rebecca Barrett. [cited by applicant]
Verreck et al., “Human IL-23-producing type 1 macrophages promote but IL-10 producing type 2 macrophages subvert immunity to (myco)bacteria,” PNAS, 2004, 101(13):4560-4565. [cited by applicant]
Wakashin et al., “IL-23 and Th17 Cells Enhance Th2-Cell-mediated Eosinophilic Airway Inflammation in Mice” American Journal of Respiratory and Critical Care Medicine, 2008, 178:1023-1032. [cited by applicant]
Wang et al,. “Antibody Structure, Instability, and Formulation,” Journal of Pharmaceutical Sciences, Jan. 1, 2007, 96(1):1-26. [cited by applicant]
Wang et al., Aggregation of Therapeutic Proteins, 2010. [cited by applicant]
Wang, Wei, “Review: Instability, stabilization, and formulation of liquid protein pharmaceuticals,” International Journal of Pharmaceutics, 1999, 185:129-188. [cited by applicant]
Wenzel, Sally, “Severe asthma: from characteristics to phenotypes to endotypes,” Clinical & Experimental Allergy, 2012, 42:650-658. [cited by applicant]
Woodle et al., “Phase I Trial of a Humanized, Fc Receptor Nonbinding OKT3 Antibody, huOKT3γ1(Ala-Ala) In the Treatment of Acute Renal Allograft Rejection,” Transplantation, 1999, 68(5):608-616. [cited by applicant]
Written Opinion dated Aug. 17, 2017, in PCT/US2016/016061. [cited by applicant]
Yannam et al., “IL-23 in Infections, Inflammation, Autoimmunity and Cancer: Possible Role in HIV-1 and AIDS,” Journal of Neuroimmune Pharmacology, 2012, 7:95-112. [cited by applicant]
Yeilding et al., “Development of the IL-12/23 antagonist ustekinumab in psoriasis: past, present and future perspectives,” Annals of the New York Academy of Sciences, 2011, 1222:30-39. [cited by applicant]
Zakharova et al., “Paradoxical Anti-Inflammatory Actions of TNF-a: Inhibition of IL-12 and IL-23 via TNF Receptor 1 in Macrophages and Dendritic Cells” Journal of Immunology, 2005, 175:5024-5033. [cited by applicant]
Bandzar et al., “Crohn's disease: A review of treatment options and current research,” Cellular Immunology, 2013, 286:45-52. [cited by applicant]
ClinicalTrials.gov study NCT02031276, published Jan. 8, 2014, 7 pages. [cited by applicant]
Ferrara et al., “Recombinant renewable polyclonal antibodies,” mABs, 2015, 7(1):32-41. [cited by applicant]
International Preliminary Report on Patentability and Written Opinion dated Oct. 16, 2018, in PCT/US2017/027332. [cited by applicant]
Jabbari et al., “Transcriptional Profiling of Psoriasis Using RNA-seq Reveals Previously Unidentified Differentially Expressed Genes,” Journal of Investigative Dermatology, 2012 (online Aug. 2011), 132:246-249. [cited by applicant]
Sands et al., “A randomized, double-blind placebo-controlled phase 2a induction study of MEDI2070 (anti-p19 antibody) in patients with active Crohn's disease who have failed anti-TNF antibody therapy,” Journal of Crohn'… [cited by applicant]
Wikipedia entry for “Guselkumab,” 5 pages, downloaded May 29, 2018. [cited by applicant]
BioPorto Product Catalog, 2010, 28 pps. [cited by applicant]
Boehringer Ingelheim, BI 655066 Dose Ranging in Psoriasis, Active Comparator Ustekinumab. Available from: https://clinicaltrials.gov/ct2/show/NCT02054481. NLM identifier. NCT 02054481. First posted Feb. 4, 2014. [cited by applicant]
Chiricozzi, A. et al., Role of IL-23 in the pathogenesis of psoriasis: a novel potential therapeutic target?, Expert Opinion Ther. Targets, vol. 18, pp. 1-13, 2014. [cited by applicant]
CircuLex Main Products Catalog, 3 pps., 2010. [cited by applicant]
Karon, A, I L-23 inhibitor topped ustenkinumab against psoriasis. M Dedge™ Rheumatology. Retrieved from www.mdedge.com/rheumatology, 3 pps. dated Apr. 2, 2015. [cited by applicant]
Usui, T., The relationship between oral mucosal immunity and activity of dental caries after prolonged strenuous exercise, Descente Sports Science, vol. 35, pp. 37-43, 2014. [cited by applicant]
Carr, T.F et al., Eosinophilic and Noneosinophilic Asthma, Am J. Respir Cirt. Care Med., vol. 197, Issue 1, pp. 22-37. (Year: 2018). [cited by applicant]
Khatri, S.B et al., Paradigms in the identification and treatment of severe persistent asthma in adults, Medscape Education Pulmonary Medicine, pp. 1-17, (Year: 2012). [cited by applicant]
Krueger et al., “Anti-IL-23A mAb BI 655066 for treatment of moderate-to-severe psoriasis: Safety, efficacy, pharmacokinetics, and biomarker results of a single-rising-dose, randomized, double-blind, placebo-controlled t… [cited by applicant]
Manning, M.C et al., Stability of Protein Pharmaceuticals: An Update, Pharmaceutical Research, vol. 27, No. 4, Apr. 2010. [cited by applicant]
Chang et al., “Practical Approaches to Protein Formulation Development,” Rational Design of Stable Protein Formulations - Theory and Practice (Carpenter et al., eds.,), Kluwer Academic/Plenum Publishers, New York, 2002,… [cited by applicant]
Bankhead et al., “Novel IL-23 Inhibitor Shows Promise in Psoriases - Interleukin-23 inhibitor has 'high efficacy, quiet safety signal',” Medpage Today, Mar. 22, 2015. [cited by applicant]
Bjorkesten, Clas-Goran af, “Monitoring treatment response in Crohn's disease,” Dissertation, Helsinki, Finland, Feb. 28, 2014, 88 pages. [cited by applicant]
European Search Report dated Jun. 5, 2020 in EP 19208511.6. [cited by applicant]
Krueger et al., “IL-17A is essential for cell activation and inflammatory gene circuits in subjects with psoriasis,” J. Allergy Clin. Immunol., 2012, 130:145-154. [cited by applicant]
Mortezavi et al., “IL12/IL23 Inhibition in the Treatment of Psoriatic Arthritis,” Curr. Treat. Options in Rheum., 2015, 1:197-209. [cited by applicant]
Partial European Search Report dated Aug. 16, 2019 in EP 19176173.3. [cited by applicant]
Tonel et al., “Cutting Edge: A Critical Functional Role for IL-23 in Psoriasis,” The Journal of Immunology, 2010, 185:5688-5691. [cited by applicant]
“A Phase III, Multicenter Study of the Efficacy and Safety of Adalimumab Treatment in Subjects With Moderate to Severe Chronic Plaque Psoriasis,” Adis Insight Trial Profile, Abbott GmbH & Co. KG, latest information upda… [cited by applicant]
“A Randomised, Double-Blind, Placebo-controlled, Proof-of-concept, Dose-ranging Study of BI 655066/ABBV-066/Risankizumab in Patients With Active Psoriatic Arthritis,” Adis Insight Trial Profile, AbbVie; Boehringer Ingel… [cited by applicant]
“An Open Label, Single Group, Long Term Safety Extension Trial of Bi 655066/ABBV-066 (Risankizumab) in Patients With Moderately to Severely Active Crohn's Disease,” Adis Insight Trial Profile, AbbVie; Boehringer Ingelhe… [cited by applicant]
“BI 655066 Versus Ustekinumab and Placebo Comparators in a Randomized Double Blind trial for Maintenance Use in Moderate to Severe Plaque Type Psoriasis-2 (UltIMMa-2),” Adis Insight Trial Profile, AbbVie; Boehringer Ing… [cited by applicant]
“Bi 655066/ABBV-066 (Risankizumab) Versus Adalimumab in a Randomized, Double Blind, Parallel Group Trial in Moderate to Severe Plaque Psoriasis to Assess Safety and Efficacy After 16 Weeks of Treatment and After Inadequ… [cited by applicant]
“Bi 655066/ABBV-066 (Risankizumab) Versus Placebo In a Multicenter Randomized Double-blind Study in Patients With Moderate to Severe Chronic Plaque Psoriasis Evaluating the Efficacy and Safety With Randomized Withdrawal… [cited by applicant]
“Bi 655066/ABBV-066 (risankizumab) Versus Ustekinumab and placebo comparators in a randomized double blind trial for Maintenance use in Moderate to severe plaque type psoriasis (UltIMMa-1),” Adis Insight Trial Profile, … [cited by applicant]
“Boehringer Ingelheim Reports Results of Phase II Head-to-Head Psoriasis Study of BI 655066,” Close-Up Media, Inc., Oct. 15, 2015, 1 page. [cited by applicant]
“Boehringer Ingelheim Updates on Phase II Psoriasis Study of BI 655066,” Close-Up Media, Inc., Mar. 25, 2015, 1 page. [cited by applicant]
“Boehringer Ingelheim's Investigational Biologic Cleared Skin Better than Ustekinumab in Head-to- Head Phase II Psoriasis Study,” Mar. 20, 2015, 14 pages. [cited by applicant]
“Efficacy and Safety of Bi 655066/ABBV-066 (Risankizumab) in Patients With Severe Persistent Asthma,” ClinicalTrials.gov, last update posted Apr. 10, 2019, 20 pages. [cited by applicant]
“Phase lla, Randomized, Double-blind, Placebo Controlled, Parallel Group Study to Assess the Safety and Efficacy of Subcutaneously Administered Bi 655066/ABBV-066 (Risankizumab) as add-on Therapy Over 24 Weeks in Patien… [cited by applicant]
“Safety, Tolerability, and Pharmacokinetics of Single Rising s.c. (Stage 1) and i.v. (Stage 2) Doses of Bi 655066/ABBV-066 (Risankizumab) in Healthy Asian and Caucasian Male Volunteers (Double-blind, Randomized, Placebo… [cited by applicant]
Ciprandi et al., “Serum IL-23 in Asthmatic Children,” Journal of Biological Regulators & Homeostatic Agents, 2012, 26(1(S)):53-61. [cited by applicant]
Feagan et al., “Efficacy and Safety of Induction Therapy With the Selective IL-23 Inhibitor BI 655066, in Patients With Moderate-to-Severe Crohn's Disease: Results of a Randomized, Double-Blind, Placebo- Controlled Phas… [cited by applicant]
Gras, J., “Guselkumab,” Drugs of the Future, 2017, 42(2):81-86. [cited by applicant]
INN risankizumab, WHO Drug Information, Jul. 10, 2015, 29(2): 195, 196, 254 and 255. [cited by applicant]
Lalovic et al., “PK-PD Analysis of PASI with Data at Boundary: BI 655066 an Anti-IL-23 mAb for the Treatment of Psoriasis,” Journal of Pharmacokinetics and Pharmacodynamics, Oct. 2015, 42(1:Suppl. 1), S64. Abstract No. … [cited by applicant]
Noda et al., “The translational revolution and use of biologics in patients with inflammatory skin diseases,” J. Allergy Clin. Immunol., 2015, 135:324-336. [cited by applicant]
Osmola-Mankowska, Angieszka, “Generalised pustular psoriasis - a case report and review of therapeutic approaches,” Przegl. Dermatol., 2014, 6(101):473-476. [cited by applicant]
Ota et al., “Phase 3 study of guselkumab, a human mAb directed against the p19 subunit of IL23, in Japanese subjects with generalized pustular psoriasis and erythrodermic psoriasis,” J. Am. Acad. Dermatol., Jun. 2017, 7… [cited by applicant]
Papp et al., “Efficacy and Safety of Different Dose Regimens of a Selective IL-23p19 Inhibitor (BI 655066) Compared with Ustekinumab in Patients with Moderate-to-Severe Plaque Psoriasis with and without Psoriatic Arthri… [cited by applicant]
Papp, Kim A., “Superior Onset and Duration of BI-655066 Compared to Ustekinumab,” European Academy of Dermatology and Venereology (EADV) 24th Annual Congress, Oct. 7-11, 2015, 767- 769. [cited by applicant]
Rasch et al., “24th European Academy of Dermatology and Venereology,” Immunotherapy, Mar. 14, 2016, 8(4):395-397. [cited by applicant]
Strober, B., “Interleukin-23 inhibition for the treatment of psoriasis: the next frontier for high-efficacy biologic therapy,” British Journal of Dermatology, 2015, 173:886-895. [cited by applicant]
Supplementary European Search Report dated Jun. 2, 2022 in EP 21191271.2. [cited by applicant]
Visvanathan et al., “IL-23 pathway inhibition by risankizumab differentially modulates the molecular and histopathological profile in psoriatic skin compared with ustekinumab,” Experimental Dermatology, 2016, 25(Suppl. … [cited by applicant]
Al-Lazikani et al., “Standard conformations for the canonical structures of immunoglobulins,” J. Mol. Biol., 1997, 273:927-948. [cited by applicant]
Altschul et al., “Basic Local Alignment Search Tool,” J. Mol. Biol., (1990), 215:403-410. [cited by applicant]
Altschul et al., “Gapped BLAST and PSI-BLAST: a new generation of protein database search programs,” Nucleic Acids Res., (1997), 25:3389-3402. [cited by applicant]
Barnes et al., “Methods for Growth of Cultured Cells in Serum-Free Medium,” Anal. Biochem., 1980, 102, 255-270. [cited by applicant]
Brennan et al., “Preparation of bispecific antibodies by chemical recombination of monoclonal immunoglobulin G1 fragments,” Science, 1985, 229:81-83. [cited by applicant]
Buchwald et al., “Long-term, continuous intravenous heparin administration by an implantable infusion pump in ambulatory patients with recurrent venous thrombosis,” Surgery, Oct. 1980, 88:507-516. [cited by applicant]
Caron et al., “Engineered humanized dimeric forms of lgG are more effective antibodies,” J. Exp. Med., Oct. 1992, 176:1191-1195. [cited by applicant]
Carter et al., “High level Escherichia coli expression and production of a bivalent humanized antibody fragment,” Bio/Technology, Feb. 1992, 10:163-167. [cited by applicant]