Rho-Kinase-IN-1 is a rho kinase inhibitor extracted from US 20090325960 A1, compound 1.008.
K-Ras G12C-IN-3 is a novel and irreversible inhibitor of mutant K-ras G12C.IC50 value:Target: K-ras G12C inhibitorFor more information, please see the following patent.Heterocyclic compounds as covalent inhibitors of G12C mutant K-Ras protein useful for treating cancers, and preparation thereofBy Ren, Pingda; Liu, Yi; Li, Liansheng; Feng, Jun; Wu, Tao From PCT Int. Appl. (2014), WO 2014152588 A1 20140925.
KRAS G12C inhibitor 55 (Compound 1) is a KRAS G12C inhibitor[1].
ML-097 (CID-2160985) is a pan Ras-related GTPases activator that can activate Rac1, cell division cycle 42, Ras, and Rab7[1].
CASIN is a selective GTPase Cdc42 inhibitor with IC50 of 2 uM. In vitro: Treatment with CASIN (5 uM) reduced the elevated level of active Cdc42 observed in aged primitive hematopoietic cells to the level observed in young cells In vivo: Reverses the aging-related and polarity phenotype of aged HSCs to that of young HSCs.
CCG-232964 is an orally active inhibitor of Rho/MRTF/SRF. CCG-232964 inhibits LPA-induced CTGF gene expression[1].
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].
Rhosin is a specific Rho inhibitor; binds to WT RhoA with an affinity ~0.4 uM Kd; does not interfere with the binding of Cdc42 or Rac1.IC50 value: 0.4 uM(binding Kd) [1]Target: RhoA inhibitorRhosin is specific to the interaction between RhoA and its GEFs including LARG, DBL, LBC, p115 RhoGEF or PDZ RhoGEF and does not interfere with the binding of Cdc42 or Rac1 to their respective GEFs. Rhosin showed a dose-dependent inhibition of endogenous RhoA activity and cell growth of MCF7 cells. Rhosin dose-dependently reduced RhoA and p-MLC1 activities of MCF7 cell-derived mammospheres with an EC50 ~30-50μM, and caused decreased size and reduced number of mammospheres in MCF7 cells [1]. Y16 works synergistically with Rhosin/G04, a Rho GTPase activation site inhibitor, in inhibiting LARG-RhoA interaction, RhoA activation, and RhoA-mediated signaling functions [2].
KRAS G12C inhibitor 13 is a KRAS G12C inhibitor extracted from patent WO2018143315A1, compound 30[1].
RMC-7977 is a reversible, tri-complex RAS inhibitor with broad spectrum activity for both mutant and wild-type (WT) KRAS, NRAS, and HRAS variants.RMC-7977 can lead to tumor regressions and was well tolerated in diverse RAS-addicted preclinical cancer models. RMC-7977 also can inhibit the growth of KRASG12C cancer models[1].