Upgrade for Complete Access See Plans and Pricing

Serving leading biopharmaceutical companies globally:

Express Scripts
Johnson and Johnson
Merck
Mallinckrodt
Moodys
Dow

Last Updated: January 28, 2022

DrugPatentWatch Database Preview

Claims for Patent: 8,715,664

➤ Subscribe for complete access

« Back to Dashboard

Summary for Patent: 8,715,664
Title:Use of human TNF.alpha. antibodies for treatment of erosive polyarthritis
Abstract: The invention describes methods of treating erosive polyarthritis comprising administering a TNF.alpha. antibody, or antigen-binding portion thereof. The invention also describes a method for testing the efficacy of a TNF.alpha. antibody, or antigen-binding portion thereof, for the treatment of erosive polyarthritis.
Inventor(s): Hoffman; Rebecca S. (Wilmette, IL), Weinberg; Mark (Wilmette, IL)
Assignee: AbbVie Biotechnology Ltd. (Hamilton, BM)
Application Number:11/435,844
Patent Litigation and PTAB cases: See patent lawsuits and PTAB cases for patent 8,715,664
Patent Claims:1. A method for inhibiting radiographic disease progression in a human subject having erosive polyarthritis associated with a disorder in which TNF.alpha. activity is detrimental, comprising administering to the subject having erosive polyarthritis an isolated human anti-TNF.alpha. antibody, or antigen-binding portion thereof, such that radiographic disease progression is inhibited in the subject, wherein a Total Sharp Score (TSS) of the subject is either maintained or decreased following administration of the human anti-TNF.alpha. antibody, or antigen-binding portion thereof, wherein the human anti-TNF.alpha. antibody, or an antigen-binding portion thereof, dissociates from human TNF.alpha. with a K.sub.d of 1.times.10.sup.-8 M or less and a K.sub.off rate constant of 1.times.10.sup.-3 s.sup.-1 or less, both determined by surface plasmon resonance, and neutralizes human TNF.alpha. cytotoxicity in a standard in vitro L929 assay with an IC.sub.50 of 1.times.10.sup.-7 M or less.

2. The method of claim 1, wherein the human anti-TNF.alpha. antibody is golimumab, or an antigen-binding portion thereof.

3. The method of claim 1, wherein the human anti-TNF.alpha. antibody, or an antigen-binding portion thereof, comprises a light chain variable region (LCVR) comprising the amino acid sequence of SEQ ID NO: 1 and a heavy chain variable region (HCVR) comprising the amino acid sequence of SEQ ID NO: 2.

4. The method of claim 1, wherein the human anti-TNF.alpha. antibody is adalimumab, or an antigen-binding portion thereof.

5. The method of claim 1, wherein the human anti-TNF.alpha. antibody, or antigen-binding portion thereof, is administered to the subject on a biweekly dosing regimen.

6. The method of claim 1, further comprising administering an additional therapeutic agent to the subject.

7. The method of claim 6, wherein the additional therapeutic agent is methotrexate.

8. A method for treating erosive polyarthritis comprising administering to a subject having erosive polyarthritis associated with a disorder in which TNF.alpha. activity is detrimental, an amount of a isolated human anti-TNF.alpha. antibody, or an antigen-binding portion thereof, such that erosive polyarthritis is treated, wherein the amount of the human TNF.alpha. antibody, or antigen-binding portion thereof, results in a statistically significant reduction or inhibition in joint damage as measured by a Total Sharp Score (TSS), wherein the human anti-TNF.alpha. antibody, or an antigen-binding portion thereof, dissociates from human TNF.alpha. with a K.sub.d of 1.times.10.sup.-8 M or less and a K.sub.off rate constant of 1.times.10.sup.-3 s.sup.-1 or less, both determined by surface plasmon resonance, and neutralizes human TNF.alpha. cytotoxicity in a standard in vitro L929 assay with an IC.sub.50 of 1.times.10.sup.-7 M or less.

9. The method of claim 8, wherein the disorder in which TNF.alpha. is detrimental is an autoimmune disease or a spondyloarthropathy.

10. The method of claim 9, wherein the autoimmune disorder is rheumatoid arthritis or juvenile rheumatoid arthritis.

11. The method of claim 9, wherein the spondyloarthropathy is ankylosing spondylitis or psoriatic arthritis.

12. The method of claim 8, further comprising administering an additional therapeutic agent to the subject.

13. The method of claim 8, wherein the additional therapeutic agent is methotrexate.

14. A method for inhibiting radiographic progression of joint disease associated with erosive polyarthritis in a subject having erosive polyarthritis associated with psoriatic arthritis or rheumatoid arthritis, said method comprising administering to the subject having erosive polyarthritis, adalimumab on a biweekly dosing regimen, such that radiographic progression is inhibited, wherein a Total Sharp Score (TSS) of the subject is maintained or decreased following administration of adalimumab.

15. The method of claim 1, wherein the disorder in which TNF.alpha. is detrimental is an autoimmune disease or a spondyloarthropathy.

16. The method of claim 15, wherein the autoimmune disease is rheumatoid arthritis, or juvenile rheumatoid arthritis.

17. The method of claim 15, wherein the spondyloarthropathy is ankylosing spondylitis or psoriatic arthritis.

18. The method of claim 8, wherein the human anti-TNF.alpha. antibody, or an antigen-binding portion thereof, comprises a light chain variable region (LCVR) comprising the amino acid sequence of SEQ ID NO: 1 and a heavy chain variable region (HCVR) comprising the amino acid sequence of SEQ ID NO: 2.

19. The method of claim 8, wherein the human anti-TNF.alpha. antibody is adalimumab, or an antigen-binding portion thereof.

20. The method of claim 8, wherein the human anti-TNF.alpha. antibody, or antigen-binding portion thereof, is administered to the subject on a biweekly dosing regimen.

21. The method of claim 8, wherein the human anti-TNF.alpha. antibody, or antigen-binding portion thereof, is administered at a dose of about 40 mg.

22. A method for treating erosive polyarthritis associated with a disorder in which TNF.alpha. activity is detrimental, said method comprising identifying a subject having erosive polyarthritis associated with a disorder in which TNF.alpha. activity is detrimental and administering to the subject an amount of an isolated human anti-TNF.alpha. antibody, or an antigen-binding portion thereof, such that erosive polyarthritis is treated, wherein the human anti-TNF.alpha. antibody, or an antigen-binding portion thereof, dissociates from human TNF.alpha. with a K.sub.d of 1.times.10.sup.-8 M or less and a K.sub.off rate constant of 1.times.10.sup.-3 s.sup.-1 or less, both determined by surface plasmon resonance, and neutralizes human TNF.alpha. cytotoxicity in a standard in vitro L929 assay with an IC.sub.50 of 1.times.10.sup.-7 M or less.

23. The method of claim 22, wherein the human anti-TNF.alpha. antibody is golimumab, or an antigen-binding portion thereof.

24. The method of claim 22, wherein the human anti-TNF.alpha. antibody, or an antigen-binding portion thereof, comprises a light chain variable region (LCVR) comprising the amino acid sequence of SEQ ID NO: 1 and a heavy chain variable region (HCVR) comprising the amino acid sequence of SEQ ID NO: 2.

25. The method of claim 22, wherein the human anti-TNF.alpha. antibody is adalimumab, or an antigen-binding portion thereof.

26. The method of claim 22, wherein the human anti-TNF.alpha. antibody, or antigen-binding portion thereof, is administered to the subject on a biweekly dosing regimen.

27. The method of claim 22, wherein the disorder is rheumatoid arthritis, or juvenile rheumatoid arthritis.

28. The method of claim 22, further comprising administering an additional therapeutic agent to the subject.

29. The method of claim 28, wherein the additional therapeutic agent is methotrexate.

30. The method of claim 1, wherein the human anti-TNF.alpha. antibody, or antigen-binding portion thereof, comprises: a light chain variable region (LCVR) comprising a CDR3 domain set forth in the amino acid sequence of SEQ ID NO: 3, or modified from SEQ ID NO: 3 by a single alanine substitution at position 1, 4, 5, 7, and/or 8 or by one to five conservative amino acid substitutions at positions 1, 3, 4, 6, 7, 8 and/or 9, a CDR2 domain set forth in the amino acid sequence of SEQ ID NO: 5, and a CDR1 domain set forth in the amino acid sequence of SEQ ID NO: 7; and a heavy chain variable region (HCVR) comprising a CDR3 domain set forth in the amino acid sequence of SEQ ID NO: 4, or modified from SEQ ID NO: 4 by a single alanine substitution at position 2, 3, 4, 5, 6, 8, 9, 10 or 11 or by one to five conservative amino acid substitutions at positions 2, 3, 4, 5, 6, 8, 9, 10, 11 and/or 12, a CDR2 domain set forth in the amino acid sequence of SEQ ID NO: 6, and a CDR1 domain set forth in the amino acid sequence of SEQ ID NO: 8.

31. The method of claim 8, wherein the human anti-TNF.alpha. antibody, or antigen-binding portion thereof, comprises: a light chain variable region (LCVR) comprising a CDR3 domain set forth in the amino acid sequence of SEQ ID NO: 3, or modified from SEQ ID NO: 3 by a single alanine substitution at position 1, 4, 5, 7, and/or 8 or by one to five conservative amino acid substitutions at positions 1, 3, 4, 6, 7, 8 and/or 9, a CDR2 domain set forth in the amino acid sequence of SEQ ID NO: 5, and a CDR1 domain set forth in the amino acid sequence of SEQ ID NO: 7; and a heavy chain variable region (HCVR) comprising a CDR3 domain set forth in the amino acid sequence of SEQ ID NO: 4, or modified from SEQ ID NO: 4 by a single alanine substitution at position 2, 3, 4, 5, 6, 8, 9, 10 or 11 or by one to five conservative amino acid substitutions at positions 2, 3, 4, 5, 6, 8, 9, 10, 11 and/or 12, a CDR2 domain set forth in the amino acid sequence of SEQ ID NO: 6, and a CDR1 domain set forth in the amino acid sequence of SEQ ID NO: 8.

32. The method of claim 14, wherein the human anti-TNF.alpha. antibody, or antigen-binding portion thereof, comprises: a light chain variable region (LCVR) comprising a CDR3 domain set forth in the amino acid sequence of SEQ ID NO: 3, or modified from SEQ ID NO: 3 by a single alanine substitution at position 1, 4, 5, 7, and/or 8 or by one to five conservative amino acid substitutions at positions 1, 3, 4, 6, 7, 8 and/or 9, a CDR2 domain set forth in the amino acid sequence of SEQ ID NO: 5, and a CDR1 domain set forth in the amino acid sequence of SEQ ID NO: 7; and a heavy chain variable region (HCVR) comprising a CDR3 domain set forth in the amino acid sequence of SEQ ID NO: 4, or modified from SEQ ID NO: 4 by a single alanine substitution at position 2, 3, 4, 5, 6, 8, 9, 10 or 11 or by one to five conservative amino acid substitutions at positions 2, 3, 4, 5, 6, 8, 9, 10, 11 and/or 12, a CDR2 domain set forth in the amino acid sequence of SEQ ID NO: 6, and a CDR1 domain set forth in the amino acid sequence of SEQ ID NO: 8.

33. The method of claim 22, wherein the human anti-TNF.alpha. antibody, or antigen-binding portion thereof, comprises: a light chain variable region (LCVR) comprising a CDR3 domain set forth in the amino acid sequence of SEQ ID NO: 3, or modified from SEQ ID NO: 3 by a single alanine substitution at position 1, 4, 5, 7, and/or 8 or by one to five conservative amino acid substitutions at positions 1, 3, 4, 6, 7, 8 and/or 9, a CDR2 domain set forth in the amino acid sequence of SEQ ID NO: 5, and a CDR1 domain set forth in the amino acid sequence of SEQ ID NO: 7; and a heavy chain variable region (HCVR) comprising a CDR3 domain set forth in the amino acid sequence of SEQ ID NO: 4, or modified from SEQ ID NO: 4 by a single alanine substitution at position 2, 3, 4, 5, 6, 8, 9, 10 or 11 or by one to five conservative amino acid substitutions at positions 2, 3, 4, 5, 6, 8, 9, 10, 11 and/or 12, a CDR2 domain set forth in the amino acid sequence of SEQ ID NO: 6, and a CDR1 domain set forth in the amino acid sequence of SEQ ID NO: 8.

Details for Patent 8,715,664

Applicant Tradename Biologic Ingredient Dosage Form BLA Approval Date Patent No. Expiredate
Abbvie Inc. HUMIRA adalimumab Injection 125057 2002-12-31 ⤷  Sign up for a Free Trial 2039-03-29
Abbvie Inc. HUMIRA adalimumab Injection 125057 2008-02-21 ⤷  Sign up for a Free Trial 2039-03-29
Abbvie Inc. HUMIRA adalimumab Injection 125057 2013-04-24 ⤷  Sign up for a Free Trial 2039-03-29
>Applicant >Tradename >Biologic Ingredient >Dosage Form >BLA >Approval Date >Patent No. >Expiredate

Make Better Decisions: Try a trial or see plans & pricing

Serving leading biopharmaceutical companies globally:

Mallinckrodt
Johnson and Johnson
Merck
Moodys
Harvard Business School
McKesson

Drugs may be covered by multiple patents or regulatory protections. All trademarks and applicant names are the property of their respective owners or licensors. Although great care is taken in the proper and correct provision of this service, thinkBiotech LLC does not accept any responsibility for possible consequences of errors or omissions in the provided data. The data presented herein is for information purposes only. There is no warranty that the data contained herein is error free. thinkBiotech performs no independent verification of facts as provided by public sources nor are attempts made to provide legal or investing advice. Any reliance on data provided herein is done solely at the discretion of the user. Users of this service are advised to seek professional advice and independent confirmation before considering acting on any of the provided information. thinkBiotech LLC reserves the right to amend, extend or withdraw any part or all of the offered service without notice.