Catalog No.
Product Name
Application
Product Information
Citations
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KRAS G12C covalent inhibitor
AMG-510 is a potent, orally bioavailable, and selective KRAS G12C covalent inhibitor with anti-tumor activity. -
KRas G12C inhibitor
KRAS G12C inhibitor 5 is a KRas G12C inhibitor extracted from patent WO2017201161A1, Compound example 147. -
KRAS G12C covalent inhibitor
AMG-510 is a potent, orally bioavailable, and selective KRAS G12C covalent inhibitor with anti-tumor activity. -
KRAS G12C inhibitor
KRAS G12C inhibitor 13 is a KRAS G12C inhibitor extracted from patent WO2018143315A1, compound 30. -
Epac inhibitor
EPAC 5376753 is an allosterically inhibitor of Epac which inhibits Epac1 with an IC50 of 4 ?M in Swiss 3T3 cells. -
K-Ras inhibitor
K-Ras-IN-1 is a K-Ras inhibitor, by binding to K-Ras in a hydrophobic pocket that is occupied by Tyr-71 in the apo-Ras crystal structure.(the detailed information refer to the reference). -
K-ras G12C inhibitor
K-Ras G12C-IN-3 is a novel and irreversible inhibitor of mutant K-ras G12C. -
covalent K-Ras G12C inhibitor
K-Ras G12C-IN-2 is an irreversible covalent K-Ras G12C inhibitor. -
K-ras G12C inhibitor
K-Ras G12C-IN-1 is a novel and irreversible inhibitor of mutant K-ras G12C extracted from patent WO 2014152588 A1. -
pan GTPase inhibitor
CID-1067700 (ML282) is a pan GTPase inhibitor, and competitively inhibits Ras-related in brain 7 (Rab7) with a Ki of 13 nM. -
RhoA subfamily Rho GTPases inhibitor
Rhosin hydrochloride is a potent, specific RhoA subfamily Rho GTPases inhibitor. -
Ras inhibitor
(rac)-Antineoplaston A10 is the racemate of Antineoplaston A10. Antineoplaston A10 is a Ras inhibitor potentially for the treatment of glioma, lymphoma, astrocytoma and breast cancer. -
Rho family GTPases inhibitor
MLS000532223 is a high affinity, selective inhibitor of Rho family GTPases, with EC50 values ranging from 16 μM to 120 μM. -
MRTF pathway inhibitor
CCG-222740 is an orally active and selective Rho/myocardin-related transcription factor (MRTF) pathway inhibitor. CCG-222740 is also a potent inhibitor of alpha-smooth muscle actin protein expression. -
S-IIP inhibitor/KRASG12C Probe
ARS-1323-Alkyne is a novel KRASG12C occupancy probe. -
HIF-1α inhibitor
PRLX-93936 dihydrochloride (Compound 16) is a small-molecule inhibitor of hypoxia-inducible factor 1α (HIF-1α) with demonstrated anticancer activity. It also suppresses signaling within the activated Ras pathway, thereby inhibiting tumor cell proliferation and survival. PRLX-93936 shows potential therapeutic relevance in the study of relapsed or refractory multiple myeloma and other Ras-driven malignancies, making it a useful compound for investigating hypoxia-related and oncogenic signaling mechanisms in cancer. -
KRAS-G12C inhibitor
BI-0474 is a potent and selective inhibitor of the KRASG12C mutant, exhibiting an IC₅₀ of 7.0 nM for disruption of the GDP–KRAS::SOS1 protein–protein interaction. It demonstrates strong antiproliferative effects in NCI-H358 cells harboring the KRASG12C mutation and displays significant antitumor efficacy in non-small cell lung cancer (NSCLC) xenograft models. Through covalent targeting of mutant KRAS, BI-0474 effectively suppresses downstream MAPK signaling, making it a valuable compound for KRAS-driven cancer research and drug development. -
EPAC antagonist
ESI-08 is a potent and selective antagonist of exchange proteins directly activated by cAMP (EPACs). It inhibits both EPAC1 and EPAC2 with an IC₅₀ of 8.4 μM, effectively blocking cAMP-induced EPAC activation while sparing cAMP-mediated protein kinase A (PKA) signaling. By selectively disrupting EPAC-dependent pathways, ESI-08 serves as a valuable tool compound for dissecting cAMP signaling mechanisms and studying EPAC-related physiological and pathological processes. -
Epac1 Inhibitor
AM-001 is a non-competitive and selective inhibitor of Epac1 (exchange protein directly activated by cAMP 1). It blocks Epac1-mediated activation of the small GTPase Rap1 in cultured cells, thereby modulating cAMP-dependent signaling pathways independent of PKA. Through inhibition of Epac1–Rap1 signaling, AM-001 has shown potential for use in cardiovascular and heart disease research, particularly in studies exploring cardiac remodeling, hypertrophy, and fibrosis. -
SOS1 activator
VUBI1 (SOS1 Activator 1) is a benzimidazole-derived small molecule that acts as a potent activator of the guanine nucleotide exchange factor SOS1, with a dissociation constant (Kᴅ) of 44 nM. It promotes RAS activation by enhancing RAS-GTP formation and modulates downstream ERK phosphorylation, thereby influencing RAS–MAPK signaling. In addition, VUBI1 serves as a functional ligand for the development of PROTAC-based degraders, such as PROTAC SOS1 Degrader-1, to induce targeted SOS1 degradation. VUBI1 is a valuable compound for studying RAS pathway regulation and its role in cancer biology. - XMU-MP-9 is a bifunctional small molecule that simultaneously targets the C2 domain of Nedd4-1 and an allosteric site on K-Ras. By bridging these two proteins, XMU-MP-9 enhances the Nedd4-1–K-Ras interaction and induces conformational changes within the complex, leading to ubiquitination and subsequent degradation of multiple mutant K-Ras isoforms. This mechanism results in the suppression of proliferation in cancer cells harboring K-Ras mutations. XMU-MP-9 is a valuable research tool for investigating the therapeutic targeting of K-Ras–driven malignancies, including colon, lung, and pancreatic cancers.
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MRTF-A/SRF Inhibitor
CCG-100602 is a selective small-molecule inhibitor of the myocardin-related transcription factor A/serum response factor (MRTF-A/SRF) signaling pathway. It specifically blocks the nuclear translocation of MRTF-A, thereby suppressing SRF-mediated transcriptional activity associated with fibrogenesis. Through this mechanism, CCG-100602 effectively downregulates profibrotic gene expression and serves as a valuable research tool for studying cytoskeletal dynamics, fibrosis, and transcriptional regulation. -
KRAS G12C inhibitor
Calderasib (MK-1084) is a highly selective inhibitor of the KRASG12C mutant, exhibiting potent antitumor activity in preclinical and clinical studies. By covalently binding to the cysteine residue within the mutant KRAS, Calderasib effectively suppresses downstream MAPK signaling and tumor cell proliferation. It can be employed as a monotherapy or in combination with immune checkpoint inhibitors such as pembrolizumab for oncology research, particularly in KRASG12C-driven cancers. -
Cdc42/Rac1 inhibitor
(R)-Ketorolac is an orally active inhibitor of the small GTPases Cdc42 and Rac1. It suppresses GTPase activity, thereby modulating signaling pathways involved in cytoskeletal dynamics and cell motility. Through this mechanism, (R)-Ketorolac alters ovarian cancer cell behaviors associated with invasion and metastasis and has been shown to alleviate cancer-associated cachexia. Its dual roles in inhibiting tumor progression and improving systemic cancer outcomes make it a promising agent for cancer research. -
GGPP synthase inhibitor
Digeranyl bisphosphonate (DGBP) is a potent inhibitor of geranylgeranyl pyrophosphate (GGPP) synthase, a key enzyme in the isoprenoid biosynthesis pathway. By blocking GGPP production, DGBP prevents the geranylgeranylation of small GTPases such as Rac1, thereby interfering with their membrane localization and downstream signaling. This mechanism makes DGBP a valuable tool compound for studying protein prenylation and related cellular processes, including cytoskeletal regulation and oncogenic signaling. -
KRASG12C inhibitor
AZD4747 is a potent and selective covalent inhibitor of the mutant GTPase KRASG12C. It exhibits excellent blood–brain barrier permeability and demonstrates strong antitumor potential in preclinical models of pancreatic and colorectal adenocarcinoma. By irreversibly binding to the cysteine residue within the KRASG12C mutant, AZD4747 effectively suppresses downstream MAPK signaling, leading to inhibition of tumor cell proliferation and survival. -
KRAS G12C inhibitor
Elisrasib (D3S-001) is an orally active KRAS^G12C inhibitor that potently inhibits the proliferation of KRAS^G12C-mutant H358 and MIA PaCa-2 cells, with IC₅₀ values of 0.6 nM and 0.44 nM, respectively. It demonstrates good metabolic stability in hepatocytes, liver microsomes, plasma, and whole blood across multiple species. Elisrasib also exhibits favorable pharmacokinetic properties and significant antitumor efficacy in mouse models. -
SOS1 inhibitor
SOS1-IN-11 is a potent small-molecule inhibitor of SOS1, exhibiting an IC₅₀ value of 30 nM. It is used in research to disrupt the SOS1–KRAS interaction and modulate RAS signaling pathways in cancer models. -
Rho/MRTF/SRF Inhibitor
CCG-232601 (compound 8f) is a potent and orally active inhibitor of the Rho/MRTF/SRF transcriptional pathway. It effectively inhibits the development of bleomycin-induced dermal fibrosis in mice and holds potential for antifibrotic research in systemic scleroderma and related fibrotic disorders. - CMC2.24 (TRB-N0224) is an orally active tricarbonylmethane compound that exhibits antitumor activity in pancreatic cancer models by inhibiting Ras activation and downstream ERK1/2 signaling. It is also a potent inhibitor of zinc-dependent matrix metalloproteinases (MMPs), with IC₅₀ values ranging from 2.0 to 69 μM. Additionally, CMC2.24 has therapeutic potential in osteoarthritis, where it restores cartilage homeostasis and reduces chondrocyte apoptosis through modulation of the NF-κB/HIF-2α pathway.
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RAS inhibitor
GDC-6036-NH is a precursor compound described in patent WO2020097537A2 and serves as a key intermediate for the synthesis of Compound 17a/b. Compound 17a/b functions as a RAS inhibitor and is suitable for use in cancer research, particularly in studies targeting RAS-driven signaling pathways. -
KRAS G12C inhibitor
AZD4625 (Compound 21) is a highly potent, selective, covalent, and allosteric inhibitor of the mutant GTPase KRAS^G12C. It exhibits strong target engagement and high oral bioavailability, making it a promising candidate for the treatment of KRAS^G12C-driven cancers. -
KRAS G12D inhibitor
HRS-4642 is a selective KRAS^G12D inhibitor with a dissociation constant (Kd) of 0.083 nM, demonstrating potent anti-cancer activity. It synergizes with Carfilzomib and exhibits strong in vivo efficacy, promoting remodeling of the tumor microenvironment into an immune-activating state.
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RAS(ON) Inhibitor
Daraxonrasib (RMC-6236) is an orally active, non-covalent RAS(ON) inhibitor that disrupts the interaction between wild-type or mutant RAS proteins and the RAS-binding domain of BRAF. It exhibits EC₅₀ values ranging from 28 to 220 nM across wild-type KRAS, NRAS, HRAS, and multiple oncogenic RAS variants. RMC-6236 inhibits pERK signaling and demonstrates anti-tumor activity in KRAS-mutant tumor models.
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pan-KRAS Inhibitor
BI-2865 is a non-covalent pan-KRAS inhibitor that binds to wild-type and mutant KRAS variants, including G12C, G12D, G12V, and G13D, with dissociation constants (K\_D) of 6.9, 4.5, 32, 26, and 4.3 nM, respectively. It inhibits the proliferation of Ba/F3 cells expressing KRAS^G12C, KRAS^G12D, or KRAS^G12V, with a mean IC₅₀ of approximately 140 nM. -
pan-KRAS inhibitor
AMG410 is a non-covalent, selective pan-KRAS inhibitor with IC₅₀ values of 1–4 nM against KRAS^G12D, KRAS^G12V, and KRAS^G13D. It demonstrates over 100-fold selectivity against HRAS and NRAS. AMG410 functions as a dual-state inhibitor, binding both GDP-bound (K\_d = 1 nM) and GTP-bound (K\_d = 22 nM) KRAS, effectively blocking signaling independent of the nucleotide state. It also inhibits proliferation in wild-type KRAS-amplified tumor cells and is suitable for research in colorectal, pancreatic, and lung cancers. -
KRAS G12C inhibitor
Divarasib (GDC-6036) is an orally bioavailable, highly potent, and selective KRAS^G12C inhibitor with an IC₅₀ of <0.01 μM. It covalently binds to the switch II (SW-II) pocket of KRAS^G12C, irreversibly locking the protein in its inactive GDP-bound conformation. -
KRAS Switch I/II Pocket Inhibitor
BI-2852 is a KRAS inhibitor designed to target the switch I/II (SI/II) pocket with nanomolar affinity. Unlike covalent KRAS^G12C inhibitors that bind the switch II pocket, BI-2852 exhibits a distinct mechanism of action and binds preferentially to active KRAS^G12D with \~10-fold greater affinity than KRAS^WT (740 nM vs. 7.5 μM). It disrupts interactions between KRAS and GEFs, GAPs, and effectors, thereby inhibiting downstream signaling and exerting antiproliferative effects in KRAS-mutant cells.
