MRTX849 is a potent, orally-available, and mutation-selective covalent inhibitor of KRAS G12C with potential antineoplastic activity. MRTX849 covalently binds to KRAS G12C at the cysteine at residue 12, locks the protein in its inactive GDP-bound conformation, and inhibits KRAS-dependent signal transduction[1][2].
Salirasib is a Ras inhibitor that inhibits specifically both oncogenically activated Ras and growth factor receptor-mediated Ras activation, resulting in the inhibition of Ras-dependent tumor growth.
TH-Z816 is a reversible inhibitor againstKRAS(G12D)mutation with an IC50 value of 14 μM, which can be used in cancer research[1].
KY1022 is a ras destabilizer. KY1022 targets the Wnt/ß-catenin pathway and inhibits development of metastatic colorectal cancer.
KRAS G12D inhibitor 16 is a KRAS G12D inhibitor. KRAS G12D inhibitor 16 has inhibitory activity against KRAS G12D and KRAS G12D mutation with IC50 value of 0.7 nM and 0.35 μM, respectively. KRAS G12D inhibitor 16 can be used for the research of many malignant tumor, such as pancreatic ductal adenocarcinomas (PDAC), colon and rectal carcinomas (CRC), non-small cell lung carcinomas (NSCLC)[1].
RMC-4998 is a molecular glue compound with good antitumor activity. RMC-4998 is able to form a ternary complex with CYPA and an activated KRAS G12C mutant. Furthermore, CYPA binding to KRAS G12C blocks the interaction between activated KRAS mutants and downstream effector proteins, thereby inhibiting signaling that promotes cell proliferation[1].
XRP44X inhibits Ras-induced transcription activation with the IC50 of 10 nM. XRP44X inhibits activation of the Ras-Erk-1/2 pathway by FGF-2[1]. XRP44X is an inhibitor of Ras/Erk activation of Elk3 that also affects microtubules[2].
Rac1-IN-3 (Compound 2) is a Rac1 inhibitor with an IC50 of 46.1 μM[1].
AZA1 is a potent dual inhibitor of Rac1 and Cdc42. AZA1 induces prostate cancer cells apoptosis and inhibits prostate cancer cells proliferation, migration and invasion[1][2].
K-Ras G12C-IN-4, compound 1, is a potent Covalent Inhibitor of KRASG12C[1].
A small molecule inhibitor of guanine nucleotide exchange factor (GEF) catalytic activity that binds to SOS1 (Kd=14.7 uM) and disrupts GEF-Ras interaction; dose-dependently disrupts the SOS1-Ras interaction by competitively inhibiting the binding of SOS1cat to GDP-bound H-Ras in a microscale thermophoresis assay; dose-dependently inhibits Ras activation and downstream ERK activation mediated through EGFR-SOS1-Ras-Raf1-MEK-ERK signaling, specifically inhibits wild-type mouse embryonic fibroblast growth but not the growth of oncogenic H-Ras(G12V)-expressing mouse embryonic fibroblasts; inhibits Ras signaling and growth of pancreatic and prostate cancer cells.
Pan KRas-IN-1 is a pan KRas inhibitor, can be used for drug resistance in cancer developed with KRas G12C inhibitors[1].
KRAS inhibitor-21 (22b) is a KRAS G12C inhibitor with an IC50 value of <0.01 μM. KRAS inhibitor-21 can be used in cancer research[1].
NSC 23766 trihydrochloride is an inhibitor of Rac1 activation.
TH-Z827 is a mutant selective KRAS(G12D) inhibitor with an IC50 of 2.4 μM. TH-Z827 does not bind KRAS(WT) or KRAS(G12C). TH-Z827 blocked the KRAS(G12D)-CRAF interaction with an IC50 value of 42 μM[1].
K-Ras G12C-IN-1 is a novel and irreversible inhibitor of mutant K-ras G12C extracted from patent WO 2014152588 A1.IC50 value:Target: K-ras G12C inhibitor
Ras modulator-1 is a modulator of Ras. Ras modulator-1 is an active compound extracted from patent US20120302581[1].
KRAS inhibitor-7 is a potent KRAS G12C inhibitor, extracted from patent WO2017087528A1, compound B[1].
KRAS G12C inhibitor 52 (Compound 7) is a KRAS G12C inhibitor[1].
Methylophiopogonanone B, homoisoflavonoid, is extracted from the root of Ophiopogon japonicas, shows high antioxidant ability[1]. Methylophiopogonanone B increases GTP-Rho and acts via the Rho signaling pathway, inducing cell morphological change via actin cytoskeletal reorganization, including dendrite retraction and stress fiber formation[2].
KRAS G12D inhibitor 6 is a potent inhibitor of KRAS G12D (extracted from patent WO2021108683A1, compound 112) [1].
GGTI298 Trifluoroacetate is a CAAZ peptidomimetic geranylgeranyltransferase I (GGTase I) inhibitor, which can inhibit Rap1A with IC50 of 3 μM; little effect on Ha-Ras with IC50 of >20 μM.
Rho-Kinase-IN-1 is a rho kinase inhibitor extracted from US 20090325960 A1, compound 1.008.
CCG-1423 is a novel inhibitor of RhoA/C-mediated gene transcription that is capable of inhibiting invasion of PC-3 prostate cancer cells in a Matrigel model of metastasis.IC50 value: 1.5 uM [1]Target: Rho signaling inhibitorin vitro: CCG-1423 selectively inhibited spontaneous PC-3 prostate cancer cell invasion through a Matrigel matrix, but not the Gαi-dependent LPA-stimulated SKOV-3 ovarian cancer cell invasion, in vitro. At 100 μM, nearly complete inhibition of invasion was achieved with a lesser degree of toxicity than that induced by CCG-1423 at 10 μM [1]. SRF binds to this site in vivo and the SRF inhibitor CCG-1423 completely blocks STARS proximal reporter activity in H9c2 cells [3]. pharmacological MKL-inhibition with CCG-1423 significantly inhibited CCN1 promoter activity as well as mRNA and protein expression[4].in vivo: Pharmacological SRF inhibition by CCG-1423 reduced nuclear MKL1 and improved glucose uptake and tolerance in insulin-resistant mice in vivo [2].
KRAS G12D inhibitor 7 is a potent inhibitor of KRAS G12D (extracted from patent WO2021108683, compound 114) [1].
SOS1-IN-3 is a potent SOS1 (son of sevenless homolog 1) inhibitor with an IC50 of 5 nM. SOS1-IN-3 has anticancer effects (WO2019122129A1; compound I-1)[1].
KRAS G12C inhibitor 51 (example 1) is a KRAS G12C inhibitor[1].
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].
RMC-6291 is an orally active and covalent inhibitor of KRASG12C(ON). RMC-6291 forms a tri-complex within tumor cells between KRASG12C(ON) and cyclophilin A (CypA). Thus, RMC-6291 prevents KRASG12C(ON) from signaling via steric blockade of RAS effector binding. RMC-6291 elicits deep and durable suppression on RAS pathway activity in KRASG12C tumor models[1].
(S)-CCG-1423 is an inhibitor of Rho signaling that blocks the nuclear import of MRTF-A. (S)-CCG-1423 reduces the nuclear accumulation of MRTF-A and improves glucose uptake and tolerance in insulin-resistance mice in vivo. (S)-CCG-1423 exhibits higher inhibition activity than the SR- and the R-isomers of CCG-1423 (HY-13991). (S)-CCG-1423 can be used for the research of cancer and diabetes[1].