Abstract: The present invention provides halofuginol, and derivatives and salts thereof, including diasteromerically enriched compositions thereof. The invention also provides pharmaceutical and cosmetic compositions thereof as well as methods for using halofuginol and derivatives thereof in treating chronic inflammatory diseases, autoimmune diseases, dry eye syndrome, fibrosis, scar formation, angiogenesis, viral infections, malaria, ischemic damage, transplant rejection, neurodegenerative diseases, T-cell neoplasms, and cosmetic conditions.

Abstract: The present invention provides novel analogs and derivatives of halofuginone. The invention also provides pharmaceutical and cosmetic compositions thereof and methods for using halofuginone analogs in treating chronic inflammatory diseases, autoimmune diseases, dry eye syndrome, fibrosis, scar formation, angiogenesis, viral infections, ischemic damage, transplant and implant rejection, neurodegenerative diseases, and cosmetic applications.

Abstract: The present invention provides novel analogs and derivatives of halofuginone. The invention also provides pharmaceutical and cosmetic compositions thereof and methods for using halofuginone analogs in treating chronic inflammatory diseases, autoimmune diseases, dry eye syndrome, fibrosis, scar formation, angiogenesis, viral infections, ischemic damage, transplant and implant rejection, neurodegenerative diseases, and cosmetic applications.

Abstract: The present invention provides halofuginol, and derivatives and salts thereof, including diasteromerically enriched compositions thereof. The invention also provides pharmaceutical and cosmetic compositions thereof as well as methods for using halofuginol and derivatives thereof in treating chronic inflammatory diseases, autoimmune diseases, dry eye syndrome, fibrosis, scar formation, angiogenesis, viral infections, malaria, ischemic damage, transplant rejection, neurodegenerative diseases, T-cell neoplasms, and cosmetic conditions.

Abstract: The present invention provides novel methods for modulating Th 17-mediated immune responses using aminoacyl tRNA synthetase inhibitors. Inhibition of aminoacyl tRNA synthetase inhibitors activates an amino acid starvation response (AAR) and can produce beneficial therapeutic effects. In some embodiments, aminoacyl tRNA synthetase inhibitors are used to treat disorders such as autoimmune diseases, graft rejection, infections, fibrosis, and inflammatory diseases.

Abstract: The present invention provides novel analogs and derivatives of halofuginone. The invention also provides pharmaceutical and cosmetic compositions thereof and methods for using halofuginone analogs in treating chronic inflammatory diseases, autoimmune diseases, dry eye syndrome, fibrosis, scar formation, angiogenesis, viral infections, ischemic damage, transplant and implant rejection, neurodegenerative diseases, and cosmetic applications.

Abstract: This invention provides methods and compositions for modulating the development and/or expansion of Th17 cells for use, for example, in the treatment of autoimmune diseases, persistent inflammatory diseases, infectious diseases and other Th17 related and/or IL-17 related diseases.

Abstract: This invention relates generally to methods and compositions for modulating the development of Th17 cells for use, for example, in the treatment of cellulite.

Abstract: This invention provides methods and compositions for modulating the formation and/or progression of cellulite and other skin disorders in a subject.

Abstract: FAST-1 and Smad2 or Smad3 form a complex that is specifically induced by signals generated by a TGF-&bgr; superfamily member. We have shown that a domain of FAST-1 directly interacts with Smad2 or Smad3, and that this interaction is mediated by specific domains of the two interacting molecules, namely, the MH2 domain of Smad2 or Smad3 and the Smad Interaction Domain (SID) of FAST-1. This result allows the development of methods and reagents for the isolation of compounds that are involved in, and/or modulate, TGF-&bgr; superfamily signalling.

Abstract: FAST-1 and Smad2 or Smad3 form a complex that is specifically induced by signals generated by a TGF-&bgr; superfamily member. We have shown that a domain of FAST-1 directly interacts with Smad2 or Smad3, and that this interaction is mediated by specific domains of the two interacting molecules, namely, the MH2 domain of Smad2 or Smad3 and the Smad Interaction Domain (SID) of FAST-1. This result allows the development of methods and reagents for the isolation of compounds that are involved in, and/or modulate, TGF-&bgr; superfamily signalling.