IgG stimulated remyelination of peripheral nerves

US10494418B2 · US · B2

Patent metadata
FieldValue
Publication numberUS-10494418-B2
Application numberUS-201715798313-A
CountryUS
Kind codeB2
Filing dateOct 30, 2017
Priority dateFeb 29, 2012
Publication dateDec 3, 2019
Grant dateDec 3, 2019

How to read this patent

A practical reading order for non-experts. Skip the full description unless you need deep technical detail.

  1. Title

    What the patent document calls the invention.

  2. Abstract

    A short plain-language summary of the technical disclosure.

  3. Assignees and inventors

    Who owns or filed the patent and who is credited as inventor.

  4. Key dates

    Filing, priority, publication, and grant dates set the timeline.

  5. First independent claim

    The legal scope of protection — read this for what is actually claimed.

  6. CPC / IPC classifications

    Technology tags used to group this patent with similar filings.

  7. Citations and related patents

    Prior art links and similar publications in this corpus.

Abstract

Official abstract text for this publication.

The present invention is based on the discovery of polyclonal IgG's ability to promote Schwann cell maturation, differentiation, and myelin production. Methods for treating non-idiopathic, demyelinating peripheral neuropathies in mammals, where the neuropathy is not immune-mediated or infection-mediated, through the administration of polyclonal IgG are provided. Types of demyelinating peripheral neuropathies treatable with the present invention include peripheral nerve trauma and toxin-induced peripheral neuropathies. Alternatively, a composition of polyclonal IgGs can be applied directly to a peripheral nerve cell to induce maturation, differentiation into a myelinating state, and myelin expression or promote cell survival.

First claim

Opening claim text (preview).

What is claimed is: 1. A method of promoting myelination of a peripheral nerve cell by a Schwann cell comprising contacting the Schwann cell with an amount of polyclonal IgG sufficient to promote myelination of the peripheral nerve cell by the Schwann cell, wherein the peripheral nerve cell is from a mammal with a demyelinating peripheral neuropathy, wherein the demyelinating peripheral neuropathy is selected from the group consisting of a trauma-induced demyelinating neuropathy, a toxin-induced demyelinating neuropathy, and an inherited demyelinating neuropathy and excludes Guillain-Barré syndrome, chronic demyelinating polyneuropathy and multifocal motor neuropathy. 2. The method of claim 1 , wherein the peripheral nerve cell is in vitro. 3. The method of claim 1 , wherein the peripheral nerve cell is in vivo. 4. The method of claim 3 , wherein the peripheral nerve cell is in a mammal with a demyelinating peripheral neuropathy. 5. The method of claim 4 , wherein said inherited neuropathy is not infection-mediated. 6. The method of claim 4 , wherein the mammal is human. 7. The method of claim 4 , wherein the polyclonal IgG is administered locally. 8. The method of claim 7 , wherein the polyclonal IgG is administered subcutaneously, intramuscularly, or intradermally. 9. The method of claim 4 , wherein the polyclonal IgG is administered systemically. 10. The method of claim 9 , wherein the polyclonal IgG is administered parenterally, intra-arterially, or intravenously. 11. The method of claim 4 , wherein an anti-inflammatory agent is co-administered with the polyclonal IgG to the mammal. 12. The method of claim 11 , wherein the anti-inflammatory agent is adrenocorticotropic hormone. 13. The method of claim 11 , wherein the anti-inflammatory agent is a corticosteroid. 14. The method of claim 11 , wherein the anti-inflammatory agent is an interferon. 15. The method of claim 11 , wherein the anti-inflammatory agent is glatiramer acetate. 16. The method of claim 11 , wherein the anti-inflammatory agent is a non-steroidal anti-inflammatory drug. 17. The method of claim 4 , wherein the polyclonal IgG is administered weekly. 18. The method of claim 4 , wherein the polyclonal IgG is administered biweekly. 19. The method of claim 4 , wherein the polyclonal IgG is administered monthly. 20. The method of claim 4 , wherein the polyclonal IgG is administered to the mammal at a dose of about 0.05 to 5 g per kg of patient body weight. 21. The method of claim 20 , wherein the polyclonal IgG is administered to the mammal at a dose of about 0.5 to 2 g per kg of patient body weight. 22. A method of promoting the differentiation of an immature Schwann cell into a myelinating state comprising contacting the Schwann cell with polyclonal IgG in an amount sufficient to induce the Schwann cell differentiation, wherein the Schwann cell is from a mammal with a demyelinating peripheral neuropathy, wherein the demyelinating peripheral neuropathy is selected from the group consisting of a trauma-induced demyelinating neuropathy, a toxin-induced demyelinating neuropathy, and an inherited demyelinating neuropathy and excludes Guillain-Barré syndrome, chronic demyelinating polyneuropathy and multifocal motor neuropathy. 23. The method of claim 22 , wherein the Schwann cell is in vitro. 24. The method of claim 22 , wherein the Schwann cell is in vivo. 25. The method of claim 24 , wherein the Schwann cell is in a mammal with a demyelinating peripheral neuropathy. 26. The method of claim 25 , wherein said inherited neuropathy is not infection-mediated. 27. The method of claim 25 , wherein the mammal is human. 28. The method of claim 25 , wherein the polyclonal IgG is administered locally. 29. The method of claim 28 , wherein the polyclonal IgG is administered subcutaneously, intramuscularly, or intradermally. 30. The method of claim 25 , wherein the polyclonal IgG is administered systemically. 31. The method of claim 30 , wherein the polyclonal IgG is administered parenterally, intra-arterially, or intravenously. 32. The method of claim 25 , wherein an anti-inflammatory agent is co-administered with the polyclonal IgG to the mammal. 33. The method of claim 32 , wherein the anti-inflammatory agent is adrenocorticotropic hormone. 34. The method of claim 32 , wherein the anti-inflammatory agent is a corticosteroid. 35. The method of claim 32 , wherein the anti-inflammatory agent is an interferon. 36. The method of claim 32 , wherein the anti-inflammatory agent is glatiramer acetate. 37. The method of claim 32 , wherein the anti-inflammatory agent is a non-steroidal anti-inflammatory drug. 38. The method of claim 25 , wherein the polyclonal IgG is administered weekly. 39. The method of claim 25 , wherein the polyclonal IgG is administered biweekly. 40. The method of claim 25 , wherein the polyclonal IgG is administered monthly. 41. The method of claim 25 , wherein the polyclonal IgG is administered to the mammal at a dose of about 0.05 to 5 g per kg of patient body weight. 42. The method of claim 41 , wherein the polyclonal IgG is administered to the mammal at a dose of about 0.5 to 2 g per kg of patient body weight. 43. A method of promoting the production of myelin by a Schwann cell comprising contacting the Schwann cell with an amount of polyclonal IgG sufficient to upregulate MBP genes, wherein the Schwann cell is from a mammal with a demyelinating peripheral neuropathy, wherein the demyelinating peripheral neuropathy is selected from the group consisting of a trauma-induced demyelinating neuropathy, a toxin-induced demyelinating neuropathy, and an inherited demyelinating neuropathy and excludes Guillain-Barré syndrome, chronic demyelinating polyneuropathy and multifocal motor neuropathy. 44. The method of claim 43 , wherein the Schwann cell is in vitro. 45. The method of claim 43 , wherein the Schwann cell is in vivo. 46. The method of claim 45 , wherein the Schwann cell is in a mammal with a demyelinating peripheral neuropathy. 47. The method of claim 46 , wherein said inherited neuropathy is not infection-mediated. 48. The method of claim 46 , wherein the mammal is human. 49. The method of claim 46 , wherein the polyclonal IgG is administered locally. 50. The method of claim 49 , wherein the polyclonal IgG is administered subcutaneously, intramuscularly, or intradermally. 51. The method of claim 46 , wherein the polyclonal IgG is administered systemically. 52. The method of claim 51 , wherein the polyclonal IgG is administered parenterally, intra-arterially, or intravenously. 53. The method of claim 46 , wherein an anti-inflammatory agent is co-administered with the polyclonal IgG to the mammal. 54. The method of claim 53 , wherein the anti-inflammatory agent is adrenocorticotropic hormone. 55. The method of claim 53 , wherein the anti-inflammatory agent is

Assignees

Inventors

Classifications

  • Drugs for specific purposes, not provided for in groups A61P1/00-A61P41/00 · CPC title

  • specific for leukemia · CPC title

  • for treating abnormal movements, e.g. chorea, dyskinesia · CPC title

  • for peripheral neuropathies · CPC title

  • Drugs for disorders of the nervous system · CPC title

Patent family

Related publications grouped by family.

External sources

Frequently asked questions

Answers are generated from the same data shown on this page.

What does patent US10494418B2 cover?
The present invention is based on the discovery of polyclonal IgG's ability to promote Schwann cell maturation, differentiation, and myelin production. Methods for treating non-idiopathic, demyelinating peripheral neuropathies in mammals, where the neuropathy is not immune-mediated or infection-mediated, through the administration of polyclonal IgG are provided. Types of demyelinating periphera…
Who is the assignee on this patent?
Baxalta Inc, Baxalta GmbH
What technology area does this patent fall under?
Primary CPC classification A61K39/39516. Mapped technology areas include Human Necessities.
When was this patent published?
Publication date Tue Dec 03 2019 00:00:00 GMT+0000 (Coordinated Universal Time) (B2). Legal status and post-grant events are not shown on this page.
What related patents are in patentsdb?
We list 8 related publications on this page (citations in our corpus or others sharing the same primary CPC).