ras-raf

Kobe0065 is a novel and effective small-molecule compound that inhibits the Ras-Raf interaction by structure-based drug design (SBDD); it displays potent activity, competitively inhibiting the binding of H-Ras·GTP to c-Raf-1 RBD with a Ki value of 46 ± 13 μM.

Kobe 2602 is an inhibitor of Ras that exhibits anticancer chemotherapeutic activities.

RAS/RAS-RAF-IN-1 is a potent inhibitor of RAS and RAS-RAF, exhibiting a KD of 5.0 μμ-15 μμ for cyclophilin A (CYPA) binding affinity and demonstrating antitumor activity[1].

Sulindac sulfide (cis-Sulindac sulfide) is a non-steroidal anti-inflammatory compound that has a high affinity for COX-1 and acts as an inhibitor in Ras activation of Raf-1. Sulindac sulfide is a non-competitive inhibitor of gamma-secretase with an IC50 value of 20.2 μM. It is an active metabolite of sulinic acid.

INU-152 is a pan-RAF inhibitor. INU-152 has potent anti-tumor activity in preclinical models of BRAFV600E mutant cancer. INU-152 inhibits all RAF isoforms and inhibits MAPK pathways in mutant BRAF cells. INU-152 exhibits minimal paradoxical pathway activa

Balamapimod is a reversible inhibitor of Ras/Raf/MEK. It also has a potential anti-tumor activity.

I194496 is an effective inhibitor of cystathionine γ-lyase (CSE) with an IC50 value of 0.79 mM. It inhibits the growth of human TNBC cells by dual targeting the PI3K/Akt and Ras/Raf/ERK pathways. Additionally, I194496 suppresses the metastasis of human TNBC cells by downregulating the Anxa2/STAT3 and VEGF/FAK/Paxillin signaling pathways.

XSJ-10 is an HDAC inhibitor containing a RAS/RAF protein interference unit, with IC50 values of 0.05 μM in PANC-1 cells and 0.04 μM in HT-29 cells. It effectively induces cancer cell apoptosis and tumor inhibition by strongly suppressing the RAS-RAF-MEK-ERK signaling pathway and HDAC3 acetylation levels.

Pan-RAS-IN-5 (compound 7A) is a molecular glue that facilitates the formation of a ternary complex with cyclophilin A (CYPA) and RAS(ON) protein. This complex inhibits the binding of RAF downstream of RAS, demonstrating antitumor activity.

Cobimetinib racemate (Cobimetinib (racemate)) (GDC-0973 racemate) is a selective inhibitor of MEK.Cobimetinib racemate is also known as a mitogen-activated protein kinase, is a key component of the RAS/RAF/MEK/ERK pathway.

Kobe2601 is a Kobe0065 and Kobe02602 water-soluble analog. It displays inhibitory activity towards Ras-Raf binding.

MCP110 is an inhibitor of the interaction of Ras with Raf-1 and can be used in studies about the treatment of human tumors.

DPQZ is an anti-tubulin compound acting by inducing cell apoptosis in human oral cancer cells through Ras/Raf inhibition and MAP kinases activation.

REDX05358 is a highly selective and potent pan RAF inhibitor with a potential therapeutic for BRAF and RAS mutant tumors. REDX05358 has improved therapeutic potential and predicted safety profile. REDX05358 demonstrates subnanomolar binding affinity for B

The Survival of Motor Neurons (SMN) protein participates in RNA splicing. Decreases in SMN, typically a consequence of defects in the smn1 gene, result in the death of motor neurons and lead to the neurodegenerative disease, spinal muscular atrophy (SMA). Cuspin-1 is a small molecule upregulator of SMN that has been shown in vitro to increase levels of SMN in SMA patient fibroblasts by 50% at 18 μM. Its mechanism of action is thought to involve increased phosphorylation of ERK to initiate Ras-Raf-MEK signaling, which results in an increased rate of SMN translation.

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).

Pan-RAF kinase inhibitor 1 is a potent inhibitor of the Pan-RAF kinase pair, which regulates MAPK signaling and affects the proliferation of RAS-mutated tumor cells. Pan-RAF kinase inhibitor 1 has shown research potential for the study of cancer diseases.

Antitumor agent-60 is a potent antitumor agent that targets the RAS-RAF signaling pathway and binds to CRAF (Kd: 721.3 nM). antitumor agent-60 increases p53 and ROS levels in cancer cells, resulting in oval and irregular nuclei. antitumor agent-60 is sufficient to block the cell cycle in G2/M phase and induce apoptosis. Antitumor agent-60 is sufficient to block the cell cycle in G2/M phase and induce apoptosis. In the A549 tumor transplantation model, Antitumor agent-60 has the ability to inhibit tumor growth.

SHR902275 is a selective, potent, orally active RAF inhibitor targeting RAS mutant cancers, acting on cRAF (IC50: 1.6 nM), bRAFwt (IC50: 10 nM), and bRAFV600E (IC50: 5.7 nM). SHR902275 exhibits cell growth inhibitory effects in H358 cells (GI50: 1.5 nM), A375 cells (GI50: 0.17 nM), Calu6 cells (GI50: 0.4 nM), and SK-MEL2 cells (GI50: 0.32 nM).

APS-2-79 hydrochloride (APS-2-79 HCl) is a MAPK antagonist that modulating KSR-dependent MAPK signalling by antagonizing RAF heterodimerization as well as the conformational changes required for phosphorylation and activation of KSR-bound MEK.

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.

APS-2-79, a KSR-dependent MEK antagonist, disrupts ATP (biotin) binding within the KSR2-MEK1 complex, achieving an inhibitory concentration (IC50) of 120 nM. This action stabilizes the KSR inactive state and antagonizes oncogenic Ras-MAPK signaling.

Deltarasin is a high affinity PDEδ-KRAS interaction inhibitor. Deltarasin can inhibit KRAS-PDEδ interactions by binding to a hydrophobic pocket on PDEδ, resulting in the impairment of cell growth, KRAS activity, and RAS/RAF signaling in human pancreatic ductal adenocarcinoma cell lines. The anti-cancer cell activity of deltarasin can be enhanced by simultaneously blocking tumor protective" autophagy

Pimasertib HCl is an orally bioavailable small-molecule inhibitor of MEK1 and MEK2 (MEK1/2) with potential antineoplastic activity. Pimasertib selectively binds to and inhibits the activity of MEK1/2, preventing the activation of MEK1/2-dependent effector proteins and transcription factors, which may result in the inhibition of growth factor-mediated cell signaling and tumor cell proliferation. MEK1/2 (MAP2K1/K2) are dual-specificity threonine/tyrosine kinases that play key roles in the activation of the RAS/RAF/MEK/ERK pathway and are often upregulated in a variety of tumor cell types.