braf in 1

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.

EGFR/BRAF-IN-1, a 2,3-dihydropyrazino[1,2-a]indole-1,4-dione derivative, is a potent inhibitor of EGFR/BRAF, inhibiting BRAFV600E (IC50:45 nM) and cancer cell proliferation (GI50=35 nM), with good antioxidant effect.

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.

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

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

Multi-kinase-IN-5 (compound 15c) is a multi-kinase inhibitory agent that shows significant inhibition against a range of protein kinases including RET, KIT, cMet, VEGFR1, VEGFR2, FGFR1, PDGFR, and BRAF, with corresponding inhibition percentages of 74%, 31%, 62%, 40%, 73%, 74%, 59%, and 69%. Its IC50 values are 1.287 μM for FGFR1, 0.117 μM for VEGFR, and 1.185 μM for RET kinases, indicating its potency [1].

CFT1946 is a selective and orally active ligand targeting BRAF kinase, functioning as a degrader of mutant BRAF forms including BRAFV600E, G469A, G466V, and p61-BRAFV600E. It is utilized in tumor research [1].

B-Raf IN 1 is a B-Raf (IC50: 24 nM) and c-Raf (IC50: 25 nM) inhibitor.

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

RAS/RAS-RAF-IN-1 is a potent RAS and RAS-RAF inhibitor. RAS/RAS-RAF-IN-1 has a KD of 5.0 μμ-15 μμ for cyclophilin A (CYPA) binding affinity. RAS/RAS-RAF-IN-1 has antitumor activity[1]. RAS/RAS-RAF-IN-1 (compound 89; for 4 hours) has an EC50 of 0.5 μμ-5.0 μμ for BRAF-GTP-KRAS-G12C disruption and has an IC50 of 1.0 μμ-10 μμ for pERK inhibition in H358 cells[1]. [1]. Meizhong Jin, et al. Compounds that participate in cooperative binding and uses thereof. WO2020132597A1.

The Immuno-Oncology Screening Library consists of 2 plates and contains more than 90 cancer and immunology-associated compounds in a 96-well Matrix tube rack format as 10 mM stock solutions in DMSO. This library includes a variety of immuno-oncology target modulators, including but not limited to, adenosine, CCR, CXCR, and TLR agonists and antagonists, BTK, PI3K, VEGFR, and BRAF inhibitors, PD-1/PDL-1 interaction inhibitors, and HDAC inhibitors. Please review the product insert for a full list of targets. Stability data is not available for the compounds as supplied in the screening library.

Rineterkib hydrochloride (compound B) is an orally active 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, BRAF-mutant NSCLC, KRAS-mutant pancreatic cancer, KRAS-mutant colorectal cancer (CRC) and KRAS-mutant ovarian cancer[1]. ERK-IN-1 (compound B) (50, 75 mg/kg, p.o., qd/q2d, 27 days) treatment significantly reduces the tumor volume in the Calu-6 human NSCLC subcutaneous tumor xenograft model in mice[1]. [1]. CAPONIGRO, et al. THERAPEUTIC COMBINATIONS COMPRISING A RAF INHIBITOR AND A ERK INHIBITOR. WO2018051306A1.