Sundeep Dugar

TL;DR: In this article, a method to inhibit TGF-β and/or p38-α kinase using compounds of formula (1) or the pharmaceutically acceptable salts thereof was proposed.

TL;DR: Significant promise is shown of the development of an effective therapeutic intervention for IPF and that inhibition of chronic progressive fibrosis may be achieved by blocking TGF-beta receptor activation.

TL;DR: TGF-β type I receptor kinase inhibitors hold promise as novel therapeutic agents for metastatic breast cancer after testing their effects on two murine mammary carcinoma cell lines in vitro and in vivo.

TL;DR: The motile and invasive properties of Smad4-deficient pancreatic cancer cells are at least partly driven by activation of endogenous TGF-β signaling, and targeting the TβR-I kinase represents a potentially powerful novel therapeutic approach for the treatment of this disease.

TL;DR: In this paper, the authors present methods to treat conditions mediated by kinase using compounds of formula (1) and the pharmaceutically acceptable salts thereof, or a pharmaceutical composition thereof, wherein Z is N or CR1, R1 is a noninterfering substituent, each of X?1 and X2? is a linker, Ar?1 or Ar2? are identical or different, and represent optionally substituted C1-C20 hydrocarbyl residues.