braf(v600e)

Lifirafenib (Beigene-283) is a potent inhibitor of RAF family kinases and EGFR in biochemical assays with IC50 of 23, 29 and 495 nM for the recombinant BRAFV600E kinase domain, EGFR and EGFR T790M/L858R mutant respectively.

PROTAC BRAF-V600E degrader-1 (Compound 23) selectively induces degradation of BRAF-V600E but not wildtype BRAF.

BRAF V600E/CRAF-IN-1 is a potent inhibitor of BRAFV600E/CRAF. BRAF V600E/CRAF-IN-1 acts in the G0/G1 phase of HCT-116 colon cancer cells to arrest the cell cycle and cause apoptosis. BRAF V600E/CRAF-IN-1 shows potential for cancer disease 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.

PROTAC BRAF-V600E degrader-2 is a useful organic compound for research related to life sciences. The catalog number is T8744 and the CAS number is 2417296-82-1.

RAF mutant-IN-1 is an inhibitor of RAF kinase(IC50 values of 21 nM, 30 nM and 392 nM for C-RAF 340D/Y341D, B-RAFV600E and B-RAFWT, respectively).

Agerafenib hydrochloride, a highly potent inhibitor of BRAFV600E (Kd: 14 nM), demonstrates significant efficacy.

HG6-64-1 is a potent and selective inhibitor of B-Raf, with an IC50 of 0.09 μM on B-raf V600E-transformed Ba/F3 cells.

Encorafenib (LGX818) is an orally available mutated BRaf V600E inhibitor(IC50=0.3 nM) with potential antineoplastic activity.

B-Raf IN 13 is a potent B-Raf inhibitor with anticancer activity, demonstrating an IC50 of 3.55 nM in the [BRAF V600E] enzyme assay.

CCT241161 is an orally active pan-RAF inhibitor, with IC50 values of 3, 6, 10, 15, and 30 nM for LCK, CRAF, SRC, V600E-BRAF, and BRAF, respectively. It exhibits significant activity against BRAF and NRAS mutant melanomas and demonstrates anticancer cell proliferative effects [1].

DS03090629, an orally active MEK inhibitor, functions by competitively inhibiting MEK activity in the presence of ATP. This compound demonstrates strong binding affinity to both MEK and phosphorylated MEK, with dissociation constants (Kd) of 0.11 and 0.15 nM, respectively. It has shown efficacy in suppressing the proliferation of melanoma cell lines that overexpress BRAF mutations, achieving IC50 values of 74.3 and 97.8 nM for BRAF V600E and MEK1 F53L transfected A375 cells, respectively. DS03090629 is thus considered promising for anti-melanoma therapies.

SJ-C1044 is an orally effective pan-RAF inhibitor demonstrating immunomodulatory and antitumor activities. It targets wild-type BRAF, wild-type CRAF, and BRAF(V600E) with IC50 values of 331, 257, and 187 nM, respectively. SJ-C1044 suppresses tumor cell proliferation by inhibiting kras activation and MEK-ERK phosphorylation. Additionally, it shows inhibition of VEGFR2, TIE2, and CSF1R, with IC50 values of 100, 23, and 235 nM respectively. The compound enhances the tumor immune microenvironment through inhibition of angiogenesis and modulation of macrophage function. SJ-C1044 is applicable for research in 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).

CST905 is an efficient PROTAC BRAF-V600E degrader with a DC50 of 18 nM, suitable for cancer research.

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.

Binimetinib (ARRY-162) is a MEK1/2 inhibitor (IC50=12 nM) with selective and oral activity. Binimetinib has antitumor activity for the treatment of metastatic melanoma that cannot be resected or has a BRAF V600E or V600K mutation.

PLX7922, a RAF inhibitor, demonstrates binding affinity with BRAF V600E and exhibits inhibitory effects on pERK in BRAF V600E cell lines, while inducing pERK activation in mutant NRAS cell lines.

Tunlametinib is a highly selective, orally bioavailable small molecule inhibitor of MEK1 and MEK2 kinases with a reported IC50 value of 1.9 nM for MEK1. Tunlametinib exerts its antitumor effects by blocking the oncogenic RAS-RAF-MEK-ERK signaling pathway, thereby inducing tumor cell cycle arrest and promoting apoptosis, Tunlametinib demonstrates strong inhibitory activity against various RAS/RAF-mutant cancer cells such as those harboring BRAF V600E or KRAS G12C mutations, shows synergistic effects in combination with BRAF/KRASG12C/SHP2 inhibitors and Docetaxel, and is used in targeted therapy for RAS/RAF-driven cancers including melanoma, colorectal cancer, and non-small cell lung cancer (NSCLC).

AZ304 is an ATP-competitive dual BRAF kinase inhibitor, effectively inhibiting BRAF (WT), BRAF (V600E), and wild-type CRAF [IC50s: 79/38/68 nM].

RO5126766 (CH5126766) is a dual RAF/MEK inhibitor with IC50 of 8.2 nM, 19 nM, 56 nM, and 160 nM for BRAF V600E, BRAF, CRAF, and MEK1, respectively. Phase 1.

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.

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.