IP Library Granted Patent US 12,358,975
Granted Patent B2
US 12,358,975 · App. 18/774,646 · Granted Jul 15, 2025

Compositions and methods for treating synucleinopathies

Inventors: Josefine Nielsen Søderberg (Valby, DK); Pekka Kallunki (Valby, DK); Louise Buur (Valby, DK); Frank Larsen (Valby, DK)
Assignee: H. Lundbeck A/S
C07K16/18A61K39/39591A61K47/22A61K47/26A61K2039/545C07K2317/92
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Quick Facts
Patent No.
US 12,358,975
App. No.
18/774,646
Granted
Jul 15, 2025
Kind
B2
Abstract

The present invention relates to stable and low viscosity liquid pharmaceutical compositions comprising antibodies binding to human alpha synuclein and to methods for use of antibodies binding to human alpha synuclein for treating synucleinopathies or prodromal synucleinopathy, incl. suitable doses and/or dosing regimens. These antibodies for use in treatment of synucleinopathies or prodromal synucleinopathy may be formulated in the stable and low viscosity liquid pharmaceutical compositions of the invention.

Claims (36)

1. A method of treating multiple system atrophy (MSA) in a human patient, the method comprising intravenously administering an anti-alpha synuclein antibody at a dose of 2100 mg or 4200 mg once every 4 weeks to the patient, wherein the antibody is a full length monoclonal human IgG1 antibody which comprises heavy chain CDR1, CDR2, and CDR3 comprising the amino acid sequences of SEQ ID NOs: 1, 34, and 3, respectively, and light chain CDR1, CDR2, and CDR3 comprising the amino acid sequences of SEQ ID NOs: 4, 5, and 6, respectively.

2. The method of claim 1 , wherein the antibody comprises a heavy chain variable domain and a light chain variable domain comprising the amino acid sequences of SEQ ID NOs: 31 and 8, respectively.

3. The method of claim 1 , wherein the antibody comprises a constant heavy chain domain comprising the amino acid sequence of SEQ ID NO: 18 and a kappa light chain constant domain comprising the amino acid sequence of SEQ ID NO: 17.

4. The method of claim 1 , wherein the binding affinity of the antibody for the oligomeric form of alpha synuclein displays approximately a 65- to 75-fold enhancement relative to the binding affinity of the antibody for the monomeric form of alpha synuclein.

5. The method of claim 1 , wherein the antibody has a half-life in the human patient of about 28-30 days.

6. The method of claim 1 , wherein the MSA is possible MSA, probable MSA, MSA type C, MSA type P, clinically established MSA, or clinically probable MSA.

7. The method of claim 1 , wherein the treatment of MSA delays disease progression.

8. The method of claim 1 , wherein the treatment of MSA delays clinical progression.

9. The method of claim 1 , wherein the antibody is administered at a dose of 2100 mg at least 3 times at about 4 weeks intervals to achieve a CSF mean steady state concentration of the antibody in the patient of at least 6 nM.

10. The method of claim 1 , wherein the antibody is administered at a dose of 4200 mg at least 3 times at about 4 weeks intervals to achieve a CSF mean steady state concentration of the antibody in the patient of at least 12 nM.

11. The method of claim 1 , wherein the antibody is administered at a dose of 2100 mg at least 3 times at about 4 weeks intervals to achieve a target engagement of oligomeric forms of alpha synuclein in the CSF of the patient of at least 90%.

12. The method of claim 1 , wherein the antibody is administered at a dose of 4200 mg at least 3 times at about 4 weeks intervals to achieve a target engagement of oligomeric forms of alpha synuclein in the CSF of the patient of at least 95%.

13. A method of treating multiple system atrophy (MSA) in a human patient, the method comprising intravenously administering an anti-alpha synuclein antibody at a dose of 2100 mg or 4200 mg once monthly to the patient, wherein the antibody is a full length monoclonal human IgG1 antibody which comprises heavy chain CDR1, CDR2, and CDR3 comprising the amino acid sequences of SEQ ID NOs: 1, 34, and 3, respectively, and light chain CDR1, CDR2, and CDR3 comprising the amino acid sequences of SEQ ID NOs: 4, 5, and 6, respectively.

14. The method of claim 13 , wherein the antibody comprises a heavy chain variable domain and a light chain variable domain comprising the amino acid sequences of SEQ ID NOs: 31 and 8, respectively.

15. The method of claim 13 , wherein the antibody comprises a constant heavy chain domain comprising the amino acid sequence of SEQ ID NO: 18 and a kappa light chain constant domain comprising the amino acid sequence of SEQ ID NO: 17.

16. The method of claim 13 , wherein the binding affinity of the antibody for the oligomeric form of alpha synuclein displays approximately a 65- to 75-fold enhancement relative to the binding affinity of the antibody for the monomeric form of alpha synuclein.

17. The method of claim 13 , wherein the antibody has a half-life in the human patient of about 28-30 days.

18. The method of claim 13 , wherein the MSA is possible MSA, probable MSA, MSA type C, MSA type P, clinically established MSA, or clinically probable MSA.

19. The method of claim 13 , wherein the treatment of MSA delays disease progression.

20. The method of claim 13 , wherein the treatment of MSA delays clinical progression.

21. The method of claim 13 , wherein the antibody is administered at a dose of 2100 mg at least 3 times at about monthly intervals to achieve a CSF mean steady state concentration of the antibody in the patient of at least 6 nM.

22. The method of claim 13 , wherein the antibody is administered at a dose of 4200 mg at least 3 times at about monthly intervals to achieve a CSF mean steady state concentration of the antibody in the patient of at least 12 nM.

23. The method of claim 13 , wherein the antibody is administered at a dose of 2100 mg at least 3 times at about monthly intervals to achieve a target engagement of oligomeric forms of alpha synuclein in the CSF of the patient of at least 90%.

24. The method of claim 13 , wherein the antibody is administered at a dose of 4200 mg at least 3 times at about monthly intervals to achieve a target engagement of oligomeric forms of alpha synuclein in the CSF of the patient of at least 95%.

25. A method of treating multiple system atrophy (MSA) in a human patient, the method comprising intravenously administering an anti-alpha synuclein antibody at a dose of 2100 mg or 4200 mg once every 4 weeks to the patient, wherein the antibody is a human IgG1, kappa antibody which comprises a heavy chain variable domain and a light chain variable domain comprising the amino acid sequences of SEQ ID NOs: 31 and 8, respectively.

26. The method of claim 25 , wherein the antibody comprises a constant heavy chain domain comprising the amino acid sequence of SEQ ID NO: 18 and a kappa light chain constant domain comprising the amino acid sequence of SEQ ID NO: 17.

27. A method of treating multiple system atrophy (MSA) in a human patient, the method comprising intravenously administering an anti-alpha synuclein antibody at a dose of 2100 mg or 4200 mg once monthly to the patient, wherein the antibody is a human IgG1, kappa antibody which comprises a heavy chain variable domain and a light chain variable domain comprising the amino acid sequences of SEQ ID NOs: 31 and 8, respectively.

28. The method of claim 27 , wherein the antibody a constant heavy chain domain comprising the amino acid sequence of SEQ ID NO: 18 and a kappa light chain constant domain comprising the amino acid sequence of SEQ ID NO: 17.

29. The method of claim 1 , wherein the treatment of MSA slows clinical progression.

30. The method of claim 29 , wherein the slowing of clinical progression is quantified by Unified Multiple System Atrophy Rating Scale (UMSARS) score.

31. The method of claim 29 , wherein the slowing of clinical progression is quantified by modified UMSARS score.

32. The method of claim 29 , wherein the slowing of clinical progression is quantified by UMSARS total score.

33. The method of claim 13 , wherein the treatment of MSA slows clinical progression.

34. The method of claim 33 , wherein the slowing of clinical progression is quantified by UMSARS score.

35. The method of claim 33 , wherein the slowing of clinical progression is quantified by modified UMSARS score.

36. The method of claim 33 , wherein the slowing of clinical progression is quantified by UMSARS total score.

Assignments (5)
ASSIGNMENT OF ASSIGNOR'S INTEREST Recorded Jul 18, 2024
From: NIELSEN SØDERBERG, JOSEFINE; KALLUNKI, PEKKA; BURR, LOUISE; LARSEN, FRANK; PARSHAD, HENRIK RAJESH KUMAR; MARKUSSEN, ANNE SOFIE
To: H. LUNDBECK A/S
Reel/Frame 068020/0627 →
ASSIGNMENT OF ASSIGNOR'S INTEREST Recorded Jul 18, 2024
From: MANNING, MARK CORNELL; KATAYAMA, DERRICK SPENCER
To: LEGACY BIODESIGN LLC
Reel/Frame 068020/0754 →
ASSIGNMENT OF ASSIGNOR'S INTEREST Recorded Jul 18, 2024
From: LEGACY BIODESIGN LLC
To: H. LUNDBECK A/S
Reel/Frame 068020/0762 →
ASSIGNMENT OF ASSIGNOR'S INTEREST Recorded Jul 18, 2024
From: GAUDEN, MAGDALENA; SMITH, JOHN
To: LONZA BIOLOGICS PLC
Reel/Frame 068020/0767 →
ASSIGNMENT OF ASSIGNOR'S INTEREST Recorded Jul 18, 2024
From: LONZA BIOLOGICS PLC
To: H. LUNDBECK A/S
Reel/Frame 068020/0832 →
Priority Claims (1)
EP 21197120 · Sep 16, 2021 · regional
Continuity (3)
Division 18341437 · Jun 26, 2023
Continuation PCTEP2022075402 · Sep 13, 2022
Related Publication 20240400662A1 · Dec 5, 2024
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