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 eciphera's kinase switch inhibitors target the mechanisms that render kinases oncogenic, retain potency against gatekeeper mutations, and afford selectivity profiles not easily attained by other approaches. |
Deciphera's BRAF Programs: selective and multi-targeted inhibitorsB-Raf kinase- Malignant melanoma/colo-rectal cancer program Partnered with Eli Lilly and Company (October 2008) DP-3346/DP-2514 preclinical Deciphera has applied its unique approach to kinase inhibitor design to BRAF kinase. It has been reported that BRAF kinase is one of the most frequently mutated members of the kinase family across all cancers, and is causative of 60+% of malignant melanomas, 40-50% of colorectal cancer, and thyroid cancers. The V600E mutant form of BRAF kinase is the dominant activating, dysregulated mutation of BRAF in these cancers. Four unique programs- Deciphera is pursuing four distinct BRAF inhibitor projects, each characterized by unique kinase inhibitory profiles. • Selective RAF inhibitors • RAF + cKIT inhibitors • RAF + KDR inhibitors • RAF + HER inhibitors DP-2514 and DP-3346 are key inhibitors from the BRAF program. These inhibitors are highly effective inhibitors of proliferation in V600E-BRAF driven tumor cell lines. Candidate inhibitors are orally bioavailable and potently inhibit the growth of V600E-BRAF tumors in mouse xenograft models. Targeting the gatekeeper mutation- Deciphera RAF inhibitors retain low nanomolar potency against the T529I gatekeeper mutant form of V600E-BRAF. This distinguishing attribute will ensure effective treatment of gatekeeper mutant variants of BRAF should they emerge resistant to other therapies.
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