IP Library Granted Patent US 9,506,058
Granted Patent B2
US 9,506,058 · App. 14/214,567 · Granted Nov 29, 2016

Compositions for treating muscular dystrophy

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Quick Facts
Patent No.
US 9,506,058
App. No.
14/214,567
Granted
Nov 29, 2016
Kind
B2
Abstract

Improved compositions and methods for treating muscular dystrophy by administering antisense molecules capable of binding to a selected target site in the human dystrophin gene to induce exon skipping are described.

Claims (29)

1. A method for treating a patient with Duchenne muscular dystrophy (DMD) in need thereof who has a mutation of the DMD gene that is amenable to exon 51 skipping, comprising intravenously administering to the patient eteplirsen at a dose of about 30 mg/kg weekly for more than 120 weeks, such that disease progression in the patient is delayed, thereby treating the patient.

2. The method according to claim 1 , wherein the patient is a pediatric patient.

3. The method according to claim 1 , wherein the patient is administered an oral corticosteroid for at least 24 weeks prior to the first dose of eteplirsen.

4. A method for reducing the loss of ambulation in a patient with Duchenne muscular dystrophy (DMD) in need thereof who has a mutation of the DMD gene that is amenable to exon 51 skipping, comprising intravenously administering to the patient eteplirsen at a dose of about 30 mg/kg weekly for more than 120 weeks, thereby reducing the loss of ambulation relative to baseline, in the patient.

5. The method according to claim 4 , wherein the patient is a pediatric patient.

6. The method according to claim 4 , wherein the patient is administered an oral corticosteroid for at least 24 weeks prior to the first dose of eteplirsen.

7. A method for restoring an mRNA reading frame to induce dystrophin protein production in a patient with Duchenne muscular dystrophy (DMD) in need thereof who has a mutation of the DMD gene that is amenable to exon 51 skipping, comprising intravenously administering to the patient eteplirsen at a dose of about 30 mg/kg weekly for more than 120 weeks, thereby restoring the mRNA reading frame to induce dystrophin protein production in the patient.

8. The method according to claim 7 , wherein the patient is a pediatric patient.

9. The method according to claim 7 , wherein the patient is administered an oral corticosteroid for at least 24 weeks prior to the first dose of eteplirsen.

10. The method of claim 4 , wherein the dystrophin protein production is measured by reverse transcription polymerase chain reaction (RT-PCR), Western blot analysis, or immunohistochemical detection.

11. The method of claim 4 , wherein ambulation is measured using the North Star Ambulatory Assessment.

12. A method for treating a patient with Duchenne muscular dystrophy (DMD) in need thereof who has a mutation of the DMD gene that is amenable to exon 51 skipping, comprising intravenously administering to the patient eteplirsen at a dose of about 30 mg/kg weekly for more than 120 weeks, such that disease progression in the patient is delayed as measured by the 6 Minute Walk Test (6MWT), thereby treating the patient.

13. A method for reducing the loss of ambulation in a patient with Duchenne muscular dystrophy (DMD) in need thereof who has a mutation of the DMD gene that is amenable to exon 51 skipping, comprising intravenously administering to the patient eteplirsen at a dose of about 30 mg/kg weekly for more than 120 weeks, thereby reducing the loss of ambulation relative to baseline in the patient as measured by the 6 Minute Walk Test (6MWT).

14. The method of claim 13 , wherein the patient loses less than 5% ambulation, relative to baseline, as measured by the 6 Minute Walk Test (6MWT) by 120 weeks.

15. The method of claim 13 , wherein the patient loses no greater than 13.9 meters walking distance relative to baseline, as measured by the 6 Minute Walk Test (6MWT) by 120 weeks.

16. The method of claim 13 , wherein the patient maintains ambulation for more than 1.5 years following treatment.

17. A method for reducing loss of pulmonary function in a patient with Duchenne muscular dystrophy (DMD) in need thereof who has a mutation of the DMD gene that is amenable to exon 51 skipping, comprising intravenously administering to the patient eteplirsen at a dose of 30 mg/kg weekly for more than 120 weeks, thereby reducing the loss of pulmonary function in the patient relative to baseline.

18. The method of claim 17 , wherein pulmonary function is measured as Maximum Inspiratory Pressure (MIP).

19. The method of claim 17 , wherein respiratory muscle function in the patient improves at least 14.6% relative to baseline pulmonary function as measured as Maximum Inspiratory Pressure (MIP).

20. The method of claim 17 , wherein pulmonary function is measured as Maximum Expiratory Pressure (MEP).

21. The method of claim 17 , wherein respiratory muscle function in the patient improves at least 15% relative to baseline pulmonary function as measured as Maximum Expiratory Pressure (MEP).

22. The method of claim 17 , wherein pulmonary function is measured as Forced Vital Capacity (FVC).

23. The method of claim 1 , wherein the patient is 7 years of age or older.

24. The method of claim 1 , further comprising administering to the patient a corticosteroid.

25. The method of claim 24 , wherein the corticosteroid is Betamethasone, Budesonide, Cortisone, Dexamethasone, Hydrocortisone, Methylprednisolone, Prednisolone, or Prednisone.

26. The method of claim 24 , wherein the corticosteroid is administered prior to, in conjunction with, or subsequent to administration of eteplirsen.

27. The method of claim 1 , further comprising confirming that the patient has a mutation in the DMD gene that is amenable to exon 51 skipping.

28. A method for treating a patient with Duchenne muscular dystrophy (DMD) in need thereof who has a mutation of the DMD gene that is amenable to exon 51 skipping, comprising intravenously administering to the patient eteplirsen at a dose of about 30 mg/kg weekly for more than 120 weeks to thereby treat DMD, wherein by 120 weeks of treatment respiratory muscle function in the patient improves at least 14.6% relative to baseline pulmonary function as measured as Maximum Inspiratory Pressure (MIP).

29. A method for treating a patient with Duchenne muscular dystrophy (DMD) in need thereof who has a mutation of the DMD gene that is amenable to exon 51 skipping, comprising intravenously administering to the patient eteplirsen at a dose of about 30 mg/kg weekly for more than 120 weeks to thereby treat DMD, wherein by 120 weeks of treatment respiratory muscle function in the patient improves at least 15% relative to baseline pulmonary function as measured as Maximum Expiratory Pressure (MEP).

Assignments (5)
SECURITY INTEREST Recorded May 7, 2025
From: SAREPTA THERAPEUTICS, INC.
To: JPMORGAN CHASE BANK, N.A. AS ADMINISTRATIVE AGENT
Reel/Frame 071218/0445 →
RELEASE OF SECURITY INTEREST Recorded Sep 16, 2022
From: BIOPHARMA CREDIT PLC
To: SAREPTA THERAPEUTICS, INC.
Reel/Frame 061120/0886 →
CORRECTIVE ASSIGNMENT TO CORRECT THE TYPOGRAPHICAL ERROR APP. NO 62/869,456 SHOULD BE CORRECTED AS 62/863,456 PREVIOUSLY RECORDED AT REEL: 051355 FRAME: 0280. ASSIGNOR(S) HEREBY CONFIRMS THE ASSIGNMENT. Recorded Jan 9, 2020
From: SAREPTA THERAPEUTICS, INC.
To: BIOPHARMA CREDIT PLC
Reel/Frame 051554/0339 →
SECURITY INTEREST Recorded Dec 23, 2019
From: SAREPTA THERAPEUTICS, INC.
To: BIOPHARMA CREDIT PLC
Reel/Frame 051355/0280 →
ASSIGNMENT OF ASSIGNOR'S INTEREST Recorded Aug 1, 2014
From: KAYE, EDWARD M
To: SAREPTA THERAPEUTICS, INC.
Reel/Frame 033443/0095 →