braf in 2

B-Raf IN 2, compound Ia, is a highly effective and specific inhibitor of BRAF. It exhibits significant potential for cancer research.

BRAF V600E/CRAF-IN-2 is a potent inhibitor of BRAFV600E/CRAF with IC50 values of 0.888 and 0.229 μM, respectively.BRAF V600E/CRAF-IN-2 induces cell cycle arrest at G0/G1 phase and apoptosis in HCT-116 colon cancer cells.BRAF V600E/CRAF-IN-2 has shown research potential for cancer disease. CRAF-IN-2 has shown potential for research into cancer disease.

VEGFR-2/BRAF-IN-1, a dual inhibitor of VEGFR-2 and BRAF kinases, demonstrates potent inhibitory activity with IC50 values of 0.049 µM for VEGFR-2, 0.063 µM for BRAF V600E, and 0.005 µM for BRAF WT. It effectively induces apoptosis and arrests the cell cycle primarily at the G1/S phase.

VEGFR-2/BRAF-IN-2, as a dual VEGFR-2 and BRAF kinase inhibitor, exhibits potent IC50 values of 0.111 µM, 0.089 µM, and 0.071 µM against VEGFR-2, BRAF V600E, and BRAF WT, respectively. This compound effectively induces apoptosis and predominantly arrests the cell cycle in the G1 phase.

Rineterkib (ERK-IN-1) is an inhibitor of RAF and ERK1/2 activating mutations in the MAPK pathway.

MEK RAF-IN-1 (Compound 16b) serves as an inhibitor targeting both MEK and RAF, demonstrating potent efficacy with IC 50 values reported at 28 nM for MEK1, and 3 nM for both BRAF and BRAFV600E. This compound exhibits significant antitumor capabilities, effectively curbing cell proliferation in vitro in MIA PaCa-2 (G12C KRAS), HCT116 (G13D KRAS), and C26 (G12D KRAS) cells. Furthermore, MEK RAF-IN-1 significantly restricts tumor growth in xenograft mouse models employed in the study of colorectal cancer.

JNK-IN-18 (compound 23b) is a potent inhibitor of JNK1, boasting an IC50 of 2 nM. It demonstrates superior efficacy when compared to its IC50 values of 125 nM for JNK2 and 98 nM for BRAF(V600E).

ERK2-IN-6 (Compound 20) is a highly selective ERK1/2 inhibitor with an IC50 value of 7.9 nM for ERK2. It effectively inhibits the proliferation of BRAFV600E mutant cells, with an IC50 of 250 nM in A375 cells. ERK2-IN-6 shows potential for research in solid tumors such as melanoma with BRAF mutations.

ERK1/2 inhibitor 10 (Compound 36c) is a potent inhibitor of ERK1 and ERK2, with IC50 values of 0.11 nM and 0.08 nM, respectively. It effectively hinders the phosphorylation of downstream substrates p90RSK and c-Myc. Additionally, ERK1/2 inhibitor 10 induces apoptosis and incomplete autophagy-related cell death. This compound demonstrates significant antitumor efficacy in models of triple-negative breast cancer and colorectal cancer harboring BRAF and RAS mutations.

SCH772984 HCl is a selective inhibitor of ERK1 2 that displays behaviors of both type I and type II kinase inhibitors, with IC50s of 4 and 1 nM, respectively. SCH772984 HCl has nanomolar cellular potency in tumor cells with mutations in BRAF, NRAS, or KRA

Rineterkib hydrochloride (compound B) is an orally active RAF and ERK1/2 inhibitor used in treating proliferative diseases characterized by activating mutations in the MAPK pathway, particularly KRAS-mutant NSCLC, BRAF-mutant NSCLC, KRAS-mutant pancreatic cancer, KRAS-mutant colorectal cancer (CRC), and KRAS-mutant ovarian cancer[1].

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.

PLX7904 (PB04), also known as PB04, is a potent and selective paradox-breaker RAF inhibitor. It is able to efficiently inhibit activation of ERK1/2 in mutant BRAF melanoma cells but does not hyperactivate ERK1/2 in mutant RAS-expressing cells.