vemurafenib

Vemurafenib (RG7204) is a B-RAF inhibitor that inhibits RAFV600E and c-RAF-1 (IC50=31 48 nM) selectively and potently. Vemurafenib exhibits antitumor activity and is used for the treatment of BRAF V600E mutation-positive melanoma.

Plx-4032 (Vemurafenib) is a small-molecule B-Raf inhibitor for the potential treatment of malignant melanoma.

Hexafluoro is an inhibitor of DRP1 phosphorylation. Honokiol DCA stimulates a phenotype suggestive of respiration through mitochondrial normalization and demonstrates activity in Vemurafenib-resistant melanoma in vivo.

Honokiol DCA is an inhibitor of DRP1 phosphorylation. Honokiol DCA stimulates a phenotype suggestive of respiration through mitochondrial normalization and demonstrating activity in Vemurafenib-resistant melanoma in vivo.

Everafenib is a potent BRAF inhibitor that crosses the blood-brain barrier and also inhibits the MAPK pathway. Everafenib inhibits the activity of a range of V600EBRAF melanoma cell lines (IC50: 2-10 nM) and is more effective than Dabrafenib and Vemurafenib. Everafenib was effective in extending the number of days of survival in a mouse model of intracranial metastatic melanoma.

EBI-907 is a highly potent and orally efficacious B-RafV600E inhibitor. EBI-907 displays a low single-digit nanomolar activity (IC50 = 4.9 nM), which is >10-fold more potent than Vemurafenib (IC50 = 59 nM). EBI-907 also exhibits high potency in selectively inhibiting the proliferation of BRAF (V600E)-dependent cell lines (A375 and Colo205) and cellular Erk phosporylation, with superior activity to Vemurafenib. EBI-907, displaying potent activity against a number of important oncogenic kinases including BRK, FGFR1, c-Kit, and PDGFRb.

Vem-L-Cy5 (compound 3), a Vemurafenib-based BRAF inhibitor conjugated with the near-infrared (NIR) fluorophore cyanine-5 (Cy5), selectively targets the BRAF V600E mutation and inhibits MEK phosphorylation. This compound demonstrates cell permeability and has been shown to inhibit the growth of various cancer cell types [1].

DETD-35 is a promising chemical compound in anti-melanoma therapy, functioning as an inhibitor of the MEK-ERK, Akt, and STAT3 signaling pathways. It enhances cancer cell apoptosis (Apoptosis) and diminishes resistance to Vemurafenib in cancer cells. The compound exhibits IC 50 values of 2.7, 6.0, 3.9, 3.1, and 2.5 μM against melanoma cell lines B16-F10, MeWo, SK-MEL-2, A2058c, and A375c, respectively. DETD-35 offers significant potential for advancing research in melanoma treatment strategies.