TBAP-001 (Synthesis 13), extracted from patent WO2015075483A1, is a pan-RAF kinase inhibitor, with an IC50 of 62 nM in BRAF V600E kinase assay[1].
B-Raf IN 7 (compound 6a) is a potent B-Raf inhibitor, with an IC50 of 110.23 nM. B-Raf IN 7 exhibits antitumor activity against colon carcinoma (HCT-116), mammary gland (MCF-7), hepatocellular carcinoma (HEPG-2), human cervical carcinoma (Hela) and human prostate cancer (PC-3) cells, with IC50 values of 7.50, 9.87, 10.57, 11.63 and 12.83 µM[1].
CCT241161 is an orally active pan-RAF inhibitor with IC50s of 3, 6, 10, 15 and 30 nM for LCK, CRAF, SRC, V600E-BRAF and BRAF, respectively. CCT241161 shows good activity to in BRAF and NRAS mutant melanomas. CCT241161 also exhibits anticancer cell proliferative activity[1].
Cyclorasin 9A5 is an 11-residue cell-permeable cyclic peptide that orthosterically inhibits the Ras-Raf protein interaction with an IC50 of 120 nM[1].
B-Raf IN 9 (compound 8b) is a potent B-Raf inhibitor, with an IC50 of 24.79 nM. B-Raf IN 9 induces apoptosis and shows cell cycle arrest at G2/M phase. B-Raf IN 9 exhibits potent antitumor activity against human prostate cancer PC-3 cell line, with an IC50 of 7.83 µM[1].
GNE-9815 is among the most highly kinase-selective RAF inhibitors targeting KRAS mutant cancers via combination treatment.
Antitumor agent-60 (compound 20) is a potent antitumor agent, targeting RAS-RAF signaling pathway and binding to CRAF with a Kd value of 3.93 μM. Antitumor agent-60 induces apoptosis by blocking cell cycle at G2/M phase. Antitumor agent-60 enhances the level of p53 and ROS. Antitumor agent-60 causes oval and irregular nucleus in cancer cells. Antitumor agent-60 can suppress the growth of tumor to some extent in A549 xenograft model[1].
ERK-IN-1 (compound B) is a RAF and ERK1/2 inhibitor in the treatment of a proliferative disease characterized by activating mutations in the MAPK pathway. The activity is particularly related to the treatment of KRAS-mutant NSCLC (non-small celllung cancer), BRAF-mutant NSCLC, KRAS-mutant pancreatic cancer, KRAS-mutant colorectal cancer (CRC) and KRAS-mutant ovanan cancer[1].
ISIS 5132 is a 20-base phosphorothioate oligonucleotide that specifically down-regulates c-raf expression.
Sorafenib (Bay 43-9006) is a potent multikinase inhibitor with IC50s of 6 nM, 20 nM, and 22 nM for Raf-1, B-Raf, and VEGFR-3, respectively.
Sorafenib tosylate is a potent multikinase inhibitor, with IC50s of 6 nM, 20 nM, and 22 nM for Raf-1, B-Raf, and VEGFR-3, respectively.
BRAF V600E/CRAF-IN-2 (Compound 9c) is a potent inhibitor of BRAF V600E/CRAF with IC50s of 0.888 and 0.229 μM, respectively. BRAF V600E/CRAF-IN-2 triggers apoptosis and cell cycle arrest at G0/G1 phase in HCT-116 colon cancer cell. BRAF V600E/CRAF-IN-2 has the potential for the research of cancer diseases[1].
Doramapimod (BIRB 796) is a highly potent p38 MAPK inhibitor with an IC50 of 4 nM. It also inhibits B-Raf with an IC50 of 83 nM.
AD57 hydrochloride is an orally active multikinase inhibitor, inhibits RET, BRAF, S6K and Src[1].
B-Raf IN 13 is a BRAF inhibitor with an IC50 of 3.55 nM in BRAF V600E enzyme assay. B-Raf IN 13 has anticaner effects (WO2020261156A1, Example 74)[1].
PROTAC RAF degrader 1 (compound 512) is a PROTAC RAF degrader. PROTAC RAF degrader 1 induces targeted degradation of BRAF mutants (DC50: 5.4 nM, 4.64 nM, 15.5 nM, 2.11 nM, 63.9 nM for BRAF V600E, V600K, G464V, G469A, K601E respectively). PROTAC RAF degrader 1 has anti-tumor activity. PROTAC RAF degrader 1 can be used for research of disorders that result from aggregation or accumulation of RAF, or the constitutive activation of RAF[1].
(Z)-GW 5074 is a compound which interacts with both mHTT (mutant huntingtin protein) and LC3, but not but not with the wild-type HTT protein. (Z)-GW 5074 inhibits c-Raf, shows no effect on autophagy, and is effective for neurodegenerative disorder[1].
AZ628 is a pan-Raf kinase inhibitor with IC50s of 105, 34 and 29 nM for B-Raf, B-RafV600E, and c-Raf-1, respectively.
RAF mutant-IN-1 is a RAF kinase inhibitor, extracted from patent WO2019107987A1, with IC50 values of 21 nM, 30 nM and 392 nM for C-RAF 340D/Y341D, B-RAFV600E and B-RAFWT, respectively[1].
EGFR/BRAFV600E-IN-1 (Compound 23) is a potent EGFR and BRAFV600E dual inhibitor with IC50s of 0.08 and 0.15 µM, respectively. EGFR/BRAFV600E-IN-1 induces apoptosis and cell cycle arrest in both pre-G1 and G2/M phases. EGFR/BRAFV600E-IN-1 exhibits antiproliferative activity againist A-549, MCF-7, Panc-1, HT-29 with IC50s of 1.2, 0.79, 1.3, and 1.23 µM, respectively[1].
MCP110 is an inhibitor of Ras/Raf-1 interaction. MCP110 blocks the interaction of Ras with Raf[1].
CEP-32496 is a highly potent and orally efficacious inhibitor of BRAFV600E with a Kd of 14 nM.
B-Raf IN 16 (Compound I) is a BRAF inhibitors that belongs a cyclic iminopyrimidine derivative. B-Raf IN 16 can be used for cancer research[1].
Tinlorafenib (PF-07284890) (compound 10) is an orally active BRAF kinase inhibitor, with IC50s of 4.25 and 2.7 nM for BRAFV600E/V600K respectively. Tinlorafenib demonstrates CNS penetration and can be used in the research of BRAF-associated malignant and benign tumors of the CNS as well as extracranial malignancies[1].
Raf inhibitor 2 is a potent raf kinase (IC50<1.0 μM) inhibitor, compound 32, extracted from patent EP1003721B1. Raf inhibitor 2 can be used for cancer research[1].
B-Raf IN 2 is a potent and selective BRAF inhibitor extracted from patent WO2021116055A1, compound Ia. B-Raf IN 2 can be used for the research of cancer[1].
LY3009120 is a pan RAF inhibitor which inhibits BRAFV600E, BRAFWT and CRAFWT with IC50s of 5.8, 9.1 and 15 nM, respectively.
Regorafenib D3 (BAY 73-4506 D3) is a deuterium labeled Regorafenib. Regorafenib is a multi-targeted receptor tyrosine kinase inhibitor[1].
Exarafenib (RAF/KIN_2787) is a potent, orally active pan-RAF inhibitor. Exarafenib has anticancer activity by suppression of downstream MAPK pathway signaling. Exarafenib can be used for cancer research[1][2].
BI-1622 is an orally active, potent and highly selective HER2 (ERBB2) inhibitor, with an IC50 of 7 nM. BI-1622 shows greater than 25-fold selectivity over EGFR. BI-1622 shows high antitumor efficacy in vivo in xenograft mouse tumor models with engineered H2170 and PC9 cells and had a favorable drug metabolism and pharmacokinetics profile[1].