US2022153737A1PendingUtilityA1
Solid forms of a compound modulating kinases
Est. expiryMay 6, 2035(~8.8 yrs left)· nominal 20-yr term from priority
A61P 17/02A61K 31/4188C07D 471/04A61P 35/00A61K 31/337A61K 31/444A61P 21/00A61P 43/00A61P 9/00A61P 29/00A61P 39/04A61P 27/02C07B 2200/13A61P 19/02A61P 17/14A61P 25/30A61K 45/06A61K 31/437A61P 1/18A61P 35/02A61K 31/436A61P 17/00A61P 25/00A61P 31/18A61P 25/32A61P 25/28A61P 27/06A61P 25/08A61K 31/352
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Abstract
Solid forms of the compound, [5-(5-chloro-1H-pyrrolo[2,3-b]pyridin-3-ylmethyl)-pyridin-2-yl]-(6-trifluoromethyl-pyridin-3-ylmethyl)-amine HCl salt (Compound I) and its free base, active on the receptor protein kinases c-Kit and/or c-Fms and/or Flt3, were prepared and characterized: Also provided are methods of using the solid forms.
Claims
exact text as granted — not AI-modified1 . (canceled)
2 . A method for treating a subject suffering from Erdheim-Chester disease comprising administering to the subject a therapeutically effective amount of a crystalline form of Compound I:
characterized by an X-ray powder diffractogram comprising peaks (±0.2°) at 7.3, 23.3 and 28.2° 2θ as determined on a diffractometer using Cu-Kα radiation.
3 . A method for treating a subject suffering from Erdheim-Chester disease comprising administering to the subject a composition comprising a therapeutically effective amount of a crystalline form of Compound I:
characterized by an X-ray powder diffractogram comprising peaks (±0.2°) at 7.3, 23.3 and 28.2° 2θ as determined on a diffractometer using Cu-Kα radiation, and a pharmaceutically acceptable excipient.
4 . The method of claim 2 , further comprising administering to the subject a therapeutically effective amount of another therapeutic agent, wherein the another therapeutic agent is: i) an alkylating agent; ii) an antibiotic; iii) an antimetabolite; iv) an antibody therapy agent; v) a hormone or hormone antagonist; vi) a taxane; vii) a retinoid; viii) an alkaloid; ix) an antiangiogenic agent; x) a topoisomerase inhibitor; xi) a protein kinase inhibitor selected from a PI3K inhibitor, Cdk4 inhibitors; an Akt inhibitor; a Mek inhibitor, a c-Kit mutant inhibitor, or an EGFR inhibitor; xii) a targeted signal transduction inhibitor; xiii) a biological response modifier; xiv) a chemotherapeutic agent; xv) an Hsp90 inhibitor; xvi) a farnesyltransferase inhibitor; xvii) an aromatase inhibitor; xvii) an IDO inhibitor; xix) a histone acetyltransferase (HAT) inhibitor; xx) histone deacetylase (HDAC) inhibitor; xxi) a sirtuin (SIRT) inhibitor; xxii) a BET inhibitor; or xxiii) an antiangiogenic agent.
5 . The method of claim 3 , further comprising administering to the subject a therapeutically effective amount of another therapeutic agent, wherein the another therapeutic agent is: i) an alkylating agent; ii) an antibiotic; iii) an antimetabolite; iv) an antibody therapy agent; v) a hormone or hormone antagonist; vi) a taxane; vii) a retinoid; viii) an alkaloid; ix) an antiangiogenic agent; x) a topoisomerase inhibitor; xi) a protein kinase inhibitor selected from a PI3K inhibitor, Cdk4 inhibitors; an Akt inhibitor; a Mek inhibitor, a c-Kit mutant inhibitor, or an EGFR inhibitor; xii) a targeted signal transduction inhibitor; xiii) a biological response modifier; xiv) a chemotherapeutic agent; xv) an Hsp90 inhibitor; xvi) a farnesyltransferase inhibitor; xvii) an aromatase inhibitor; xvii) an IDO inhibitor; xix) a histone acetyltransferase (HAT) inhibitor; xx) histone deacetylase (HDAC) inhibitor; xxi) a sirtuin (SIRT) inhibitor; xxii) a BET inhibitor; or xxiii) an antiangiogenic agent.Cited by (0)
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