Catalog No.
Product Name
Application
Product Information
Citations
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KRAS G12C inhibitor
Opnurasib (JDQ-443, also known as NVP-JDQ443) is an orally active, potent, selective, and covalent KRAS^G12C inhibitor, as described in patent WO2021120890A1. It exhibits strong antitumor activity in KRAS^G12C-driven cancer models. -
ULK1/2 inhibitor
DCC-3116 is an orally active inhibitor of ULK1/2 that suppresses autophagy in lung cancer cells. By targeting ULK1/2, DCC-3116 inhibits KRAS^G12C-driven signaling pathways, leading to reduced cell proliferation and demonstrating anti-tumor activity in KRAS-mutant lung cancer models. -
TrxR-1 inhibitor
Manumycin A is a polyketide antibiotic that functions as an inhibitor of thioredoxin reductase 1 (TrxR-1). It exhibits anti-tumor activity by inhibiting breast cancer cell growth, potentially through LC3-mediated mechanisms. Manumycin A also downregulates pro-inflammatory cytokine release in TNF-α-stimulated human monocytes, indicating anti-inflammatory potential. Additionally, it inhibits the Ras/Raf/ERK1/2 signaling pathway and hnRNP H1 in castration-resistant prostate cancer cells, thereby suppressing exosome biogenesis and secretion. -
RAS-G12V inhibitor
RMC-5127 is an orally active, brain-penetrant, mutant-selective tri-complex inhibitor targeting RASG12V. It non-covalently binds to cyclophilin A (CypA), forming a binary complex that engages active RASG12V to create a high-affinity tri-complex, thereby sterically blocking RAS-effector interactions. RMC-5127 inhibits RAS signaling in KRASG12V-mutant cancer cells, suppressing proliferation and inducing apoptosis. It holds promise for the study of RAS-mutant cancers, including non-small cell lung cancer. -
KRAS G12D inhibitor
MRTX1133 is a noncovalent, potent, and selective KRAS G12D inhibitor featuring an alkyne-based structure. It binds with high affinity to the switch II pocket of KRAS G12D, with an estimated KD of 0.2 pM, engaging three key substituents that enhance protein interactions. MRTX1133 inhibits SOS1-mediated nucleotide exchange and disrupts formation of the KRAS G12D/GTP/RAF1 complex, thereby blocking downstream mutant KRAS signaling. It selectively targets KRAS G12D mutant cells without affecting KRAS wild-type cells, exhibiting single-digit nanomolar potency in cellular assays and strong antitumor efficacy in KRAS G12D-driven in vivo models. -
RAS inhibitor
ADT-007 is a potent and orally active pan-RAS inhibitor with strong anticancer activity. It binds to RAS in its nucleotide-free conformation, effectively blocking GTP loading and activation. ADT-007 selectively inhibits the proliferation of cancer cells harboring mutated or hyperactivated wild-type RAS isozymes, making it a promising candidate for RAS-driven cancer research and therapy. -
KRAS G12C inhibitor
Fulzerasib (GFH925) is an irreversible inhibitor of KRAS^G12C, demonstrating potent anticancer activity. It exhibits synergistic effects when combined with cetuximab, enhancing the therapeutic efficacy against KRAS^G12C-driven tumors. -
SOS1 inhibitor
RGT-018 is a potent, orally active SOS1 inhibitor that exhibits anti-tumor activity by blocking KRAS activation. By disrupting the SOS1–KRAS interaction, RGT-018 effectively inhibits cancer cell proliferation, making it a promising candidate for targeting KRAS-driven malignancies. -
KRAS G12C inhibitor 36
Glecirasib (Compound 1-2; JAB-21822) is a potent and orally active inhibitor of KRAS^G12C. As a member of the Ras protein family—key regulators of intracellular signaling involved in cell growth and development—KRAS^G12C is a critical oncogenic driver. Glecirasib shows strong potential for the study and treatment of KRAS^G12C-mediated cancers. -
Ras-related GTPases activator
ML-099 (CID-888706) is a pan Ras-related GTPase activator that promotes the activation of multiple small GTPases, including Rac1, Cdc42, Ras, Rab7, and Rab2A. It serves as a useful tool for studying the regulation and function of Ras-related GTPase signaling pathways. -
KRAS G12D inhibitor
Zoldonrasib (RMC-9805) is a potent, orally active inhibitor selectively targeting KRAS^G12D. It induces apoptosis in KRAS^G12D-mutant cancer cells and holds significant potential for the study and treatment of KRAS^G12D-driven malignancies. -
KRAS G12C inhibitor
Olomorasib is a potent and selective inhibitor of KRAS^G12C, demonstrating significant tumor growth inhibition, as reported in patent WO2021118877A1. It is under investigation for targeted therapy in KRAS^G12C-mutant cancers -
KRASG12C inhibitor
RMC-4998 is an orally active inhibitor that selectively targets the active, GTP-bound state of the KRAS^G12C mutant. It forms a ternary complex with intracellular cyclophilin A (CYPA) and activated KRAS^G12C, exhibiting an IC50 of 28 nM. RMC-4998 suppresses ERK signaling and induces apoptosis in KRAS^G12C-mutant cancer cells, making it a valuable candidate for tumor research. -
RAS inhibitor
RMC-7977 is an orally bioavailable, triple-complex RAS inhibitor that functions by simultaneously binding to cyclophilin A (CypA; K_d = 195 nM) and KRAS^G12V (K_d = 292 μM), facilitating the formation of a stable inhibitory complex. It exhibits broad-spectrum activity against RAS isoforms—including KRAS, NRAS, and HRAS—across both wild-type and mutant variants. RMC-7977 suppresses key oncogenic signaling pathways by inhibiting the phosphorylation of ERK, CRAF, and RSK, while promoting apoptosis through enhanced PARP cleavage. This dual mechanism results in significant tumor regression and reduced acquired resistance in KRAS^G12C-driven cancer models. It also shows favorable tolerability across a range of RAS-mutant tumor models, positioning it as a promising therapeutic candidate for RAS-driven malignancies. -
KRAS-G12C(ON) Inhibitor
Elironrasib is an orally active, covalent inhibitor specifically targeting the active GTP-bound form of KRAS^G12C (KRAS^G12C(ON)). It uniquely functions by forming a stable tri-complex with KRAS^G12C(ON) and cyclophilin A (CypA) within tumor cells, leading to steric hindrance that blocks the interaction between KRAS and its downstream effectors. This mechanism effectively suppresses RAS-mediated signaling, particularly the ERK pathway. Elironrasib induces apoptosis in KRAS^G12C-mutant H358 non-small cell lung cancer cells and demonstrates potent antiproliferative activity across KRAS^G12C-mutant cell lines, with a median IC₅₀ of 0.11 nM. Its high specificity and novel mechanism make it a promising therapeutic candidate for cancers driven by KRAS^G12C mutations. -
KRAS/ERK/RAS Inhibitor
LUNA18 is an orally bioavailable cyclic peptide that functions as a dual inhibitor of KRAS and ERK signaling pathways. It disrupts the interaction between RAS and guanine nucleotide exchange factors (GEFs), effectively inhibiting RAS activation and downstream signaling. In RAS-mutated cancer cells, LUNA18 reduces cell proliferation while modulating key signaling nodes, including phosphorylation of ERK and AKT. In preclinical studies, LUNA18 demonstrates potent anticancer activity, particularly in xenograft models, by blocking RAS-driven tumor growth. It shows significant cellular efficacy against cancer cell lines harboring KRAS mutations, including colon, gastric, pancreatic, and non-small cell lung cancers, highlighting its therapeutic potential as a targeted agent for RAS-driven malignancies. -
PROTAC SOS1 degrader
PROTAC SOS1 Degrader-1 (TFA) is a potent PROTAC molecule targeting SOS1, with a DC₅₀ of 98.4 nM. It exhibits antiproliferative activity in cancer cells harboring various KRAS mutations and demonstrates antitumor efficacy with low toxicity, making it a promising candidate for targeted cancer therapy research. -
PROTAC KRAS G12C Degrader
LC-2 is a first-in-class, VHL-based PROTAC designed to degrade endogenous KRAS G12C. Incorporating a MRTX849-derived covalent warhead, LC-2 binds KRAS G12C and recruits the VHL E3 ligase, inducing rapid and sustained degradation with DC₅₀ values between 0.25 and 0.76 μM. It effectively suppresses MAPK signaling in both homozygous and heterozygous KRAS G12C mutant cell lines, making it a valuable tool for targeted cancer research. -
PROTAC K-Ras Degrader
PROTAC K-Ras Degrader-1 (Compound 518) is a cereblon-based PROTAC that selectively degrades K-Ras, achieving ≥70% degradation efficiency in SW1573 cells. It serves as a valuable tool for studying K-Ras-driven signaling pathways and potential therapeutic strategies in cancer research. -
KRAS G12D PROTAC Degrader
Setidegrasib is a PROTAC degrader specifically targeting the KRAS G12D mutation with a DC50 of 37 nM. This compound effectively induces the degradation of KRAS G12D protein, leading to the suppression of key signaling molecules such as p-ERK, p-AKT, and p-S6 in AsPC-1 cells. Setidegrasib demonstrates significant anti-tumor activity across various cancer xenograft models, making it a valuable tool for studying KRAS(G12D)-mutated solid tumors. -
KRAS degrader
ACBI3 is a PROTAC designed to target KRAS, employing a unique mechanism to induce degradation of this oncogenic protein. It comprises a pan-KRAS degrader linked to an E3 ligase ligand through a specialized linker, facilitating the recruitment of the proteasome for degradation. ACBI3 has demonstrated significant biological activity by achieving durable modulation of signaling pathways and promoting tumor regression in KRAS mutant xenograft mouse models, making it a valuable tool for research into cancer therapeutics aimed at KRAS-driven malignancies. -
PROTAC KRAS G12D Degrader
PROTAC KRAS G12D degrader 1 functions as a selective PROTAC targeting the KRAS G12D mutant by promoting its degradation. This compound effectively inhibits the proliferation of KRAS G12D-mutant cell lines and suppresses phosphorylation of ERK, a critical pathway in cancer signaling. In vivo studies demonstrate its ability to impede tumor growth in mice with AsPC-1 xenografts, making it a valuable tool for research into KRAS G12D-driven cancers. -
SOS1 Inhibitor
SOS1-IN-14 is a potent and selective inhibitor of SOS1, demonstrating an IC50 value of 3.9 nM. This orally active compound is absorbed in the intestine through a P-glycoprotein-mediated efflux mechanism. SOS1-IN-14 is primarily utilized in research on KRAS-mutated cancers, showcasing superior tumor suppression capabilities compared to alternative therapies. -
Rac1 Inhibitor
Rac1-IN-4 is a selective inhibitor of Rac1, a Rho GTPase involved in various cellular processes including cytoskeletal dynamics and cell migration. This compound effectively disrupts the signaling pathways mediated by Rac1, making it a valuable tool for studying cancer metastasis and neurodegenerative diseases. Rac1-IN-4 is utilized in research to explore the therapeutic potential of targeting Rac1 in cellular signaling and pathology. -
Ras Inhibitor
ASP2453 is a selective and orally bioavailable inhibitor targeting the KRAS G12C mutation. It functions by inhibiting the interaction between KRAS G12C and Raf mediated by Son of Sevenless (SOS), demonstrating an IC50 value of 40 nM. ASP2453 shows potential in cancer research, particularly in studies addressing KRAS-driven malignancies. -
K-Ras Inhibitor
KRpep-2d is a potent inhibitor of K-Ras, targeting the K-Ras signaling pathway known for its role in various cancers. This compound effectively reduces the proliferation of K-Ras-driven cancer cells, making it a valuable tool for cancer research. Its application can aid in the development of therapeutic strategies for K-Ras-associated malignancies. -
SOS1/KRAS Inhibitor
SAH-SOS1A TFA is a peptide-based inhibitor targeting the SOS1-KRAS protein interaction. It exhibits nanomolar affinity for both wild-type and various mutant KRAS forms, including G12D, G12V, G12C, G12S, and Q61H (EC50 = 106-175 nM). By directly disrupting nucleotide association, SAH-SOS1A TFA effectively impairs KRAS-driven cancer cell viability and inhibits the downstream ERK-MAPK phosphosignaling cascade, making it a valuable tool for research in cancer biology. -
SOS1 Inhibitor
SOS1-IN-15 is a potent SOS1 inhibitor with an IC50 value of 5 nM, designed to specifically target and inhibit SOS1 activity. Its strong inhibitory effect makes it a promising candidate for research into KRAS-driven cancers, facilitating the understanding of oncogenic signaling pathways and development of targeted therapeutic strategies. -
Anticancer Agent
ARN22089 is a novel trisubstituted pyrimidine that acts as an anticancer agent by inhibiting the interaction of CDC42 GTPases with downstream effectors. This mechanism disrupts critical signaling pathways involved in tumorigenesis. In preclinical studies, ARN22089 has demonstrated the ability to inhibit tumor growth in a BRAF mutant mouse melanoma model, making it a valuable compound for research in cancer therapeutics and signaling pathways. -
KRASG12C Inhibitor
RM-018 is a potent KRASG12C inhibitor that specifically targets the GTP-bound, active state of KRASG12C. This tricomplex compound effectively inhibits KRASG12C/Y96D, showcasing its potential to overcome resistance mechanisms. RM-018 is an invaluable tool for studying KRAS-related signaling pathways and developing targeted therapies in cancer research. -
NRAS Proto-oncogene Expression Reducer
RGB-1 is a selective RNA G-quadruplex stabilizer that targets and reduces the expression of the NRAS proto-oncogene within breast cancer cells. This compound serves as a valuable tool for exploring the cellular mechanisms and functions of RNA G-quadruplex structures, while also aiding in the identification of novel mRNA sequences capable of forming G-quadruplexes. RGB-1 is particularly relevant for research focused on breast cancer therapeutics and the molecular basis of oncogene regulation. -
Ras Activator
Methylophiopogonanone B is a homoisoflavonoid that serves as a Ras activator. Isolated from the root of Ophiopogon japonicus, it exhibits potent antioxidant properties. This compound enhances GTP-Rho levels and activates the Rho signaling pathway, thereby inducing morphological changes in cells, such as actin cytoskeletal reorganization, dendrite retraction, and stress fiber formation. It is a valuable reagent for research into cellular signaling and structural dynamics. -
Rac1/Cdc42 Inhibitor
AZA1 is a potent dual inhibitor of Rac1 and Cdc42, key regulators of cell signaling pathways. This compound has been shown to induce apoptosis in prostate cancer cells while simultaneously inhibiting their proliferation, migration, and invasion. AZA1 serves as a valuable tool for research into the molecular mechanisms of prostate cancer progression and potential therapeutic interventions. -
Cdc42 Inhibitor
MLS-573151 is a selective inhibitor of the GTPase Cdc42, exhibiting an EC50 of 2 μM. It specifically targets Cdc42 without affecting other members of the GTPase family, such as Rab2, Rab7, H-Ras, Rac1, Rac2, and wild-type RhoA. By inhibiting GTP binding to Cdc42, MLS-573151 serves as a valuable tool for studying cellular processes regulated by this signaling pathway. Its application is essential in research related to cancer and other diseases where Cdc42 plays a critical role in cell migration and proliferation. -
Rac1 Inhibitor
Z62954982 is a selective Rac1 inhibitor with an IC50 of 12 μM, demonstrating notable potency in disrupting the Rac1/Tiam1 complex. This compound effectively reduces active Rac1 levels (GTP-bound) in the cytoplasm while preserving the function of other Rho GTPases such as Cdc42 and RhoA. Z62954982 serves as a valuable tool for studies investigating Rac1-mediated signaling pathways and their role in various biological processes. -
Tyrosinase Inhibitor
Norartocarpetin is a potent tyrosinase inhibitor, demonstrating significant inhibition with an IC50 value of 0.47 μM. This compound serves as an effective antibrowning agent for food systems research and exhibits notable anticancer activity against lung carcinoma cells (NCI-H460) with an IC50 of 22 μM. Its antiproliferative effects are mediated through targeting the Ras/Raf/MAPK signaling pathway, inducing mitochondrial-mediated apoptosis, causing S-phase cell cycle arrest, and inhibiting cell migration and invasion in human lung carcinoma cells. -
Ras-related GTPases Activator
ML-097 is a potent activator of Ras-related GTPases, specifically targeting Rac1, CDC42, Ras, and Rab7. It plays a critical role in modulating cellular signaling pathways associated with proliferation, migration, and cytoskeletal organization. This compound is valuable for research applications focusing on cancer biology, neurobiology, and cellular communication mechanisms. -
RAS-Effector PPI Inhibitor
RAS inhibitor Abd-7 is a selective RAS-binding compound (Kd=51 nM) that disrupts RAS-effector protein-protein interactions. This inhibitor effectively interferes with RAS-dependent signaling pathways by preventing the interactions between RAS and key effectors such as PI3K, CRAF, and RALGDS, as well as mutant KRAS proteins, NRAS Q61H, and HRAS G12V. RAS inhibitor Abd-7 is valuable for research applications targeting RAS-mediated processes in cancer biology. -
KRAS(G12C) Inhibitor
BBO-8520 is a selective covalent inhibitor of the KRAS G12C mutation, effectively promoting the inactive (OFF) state of KRAS by blocking GTP binding. This compound inhibits cell proliferation and disrupts the interaction between RAS and RAF1, leading to significant impact on oncogenic signaling pathways. BBO-8520 is suitable for research applications focusing on cancer biology and therapeutic strategies targeting KRAS-driven tumors. -
Rab27a-JFC1 Inhibitor
Nexinhib20 is a selective inhibitor of the Rab27a-JFC1 interaction (IC50: 2.6 μM) and Rac-1-GTP signaling. This compound effectively inhibits neutrophil exocytosis, adhesion, and β2 integrin activation, demonstrating significant anti-inflammatory properties. Nexinhib20 is suitable for research applications focused on systemic inflammation and myocardial ischemia-reperfusion injury. -
Epac Activator
8-pCPT-2′-O-Me-cAMP sodium is an analog of cyclic AMP that serves as a selective activator of exchange proteins activated by cAMP (Epac). This compound demonstrates effective activation of Epac1 with an EC50 value of 2.2 μM, while showing minimal activity towards protein kinase A (EC50 >10 μM). In vitro studies highlight its role in stimulating Epac-mediated Ca2+ release in pancreatic β-cells, and it functions as an activator of Rap1. Additionally, 8-pCPT-2′-O-Me-cAMP sodium has been shown to strengthen the barrier of retinal pigment epithelium against pathological choroidal endothelial cell invasion, contributing to research on macular degeneration. -
KRas Inhibitor
Pan KRas-IN-1 is a pan KRas inhibitor that targets mutant KRas proteins, particularly effective against KRas G12C inhibitor-resistant cancer models. It exhibits potent anti-cancer activity by disrupting KRas signaling pathways, thereby inhibiting tumor cell proliferation and survival. This compound is valuable in research applications focused on overcoming resistance mechanisms in KRas-driven malignancies. -
PROTAC KRAS G12C Degrader
PROTAC KRAS G12C degrader-1 is a Cereblon-based PROTAC targeting the KRAS G12C mutant. This compound promotes the formation of a dimer between Cereblon and KRAS G12C, leading to the degradation of GFP-tagged KRAS G12C in reporter cell systems. It serves as a valuable tool for research on targeted degradation strategies in KRAS-driven cancers. -
Cdc42 GTPase Inhibitor
ML141 (CID-2950007) is a potent, allosteric, selective and reversible non-competitive inhibitor of Cdc42 GTPase. ML141 inhibits Cdc42 wild type and Cdc42 Q61L mutant with EC50s of 2.1 and 2.6 μM, respectively. ML141 shows low micromolar potency and selectivity against other members of the Rho family of GTPases (Rac1, Rab2, Rab7). ML141 do not show cytotoxicity in multiple cell lines. -
PI3K/Akt/Ras/Raf/MAPK Inhibitor
Erufosine is a potent inhibitor of the PI3K/Akt and Ras/Raf/MAPK signaling pathways. It demonstrates significant cytotoxic activity against breast cancer cell lines, specifically MCF-7 and MDA-MB-231, with IC50 values of 40.95 μM and 40.8 μM, respectively. By reducing the phosphorylation levels of PI3K (p85), Akt (PKB), and cRaf, Erufosine serves as a valuable tool in the research of breast cancer and myeloid leukemia. -
pan-KRAS Inhibitor
pan-KRAS-IN-5 is a pan-KRAS inhibitor that functions by targeting 5′-UTR RNA G-quadruplexes (rG4s). It effectively binds to and stabilizes KRAS rG4s, leading to the inhibition of KRAS translation and downstream signaling via the MAPK and PI3K-AKT pathways. This compound has been shown to induce cell cycle arrest and promote apoptosis in KRAS-driven cancer cells, while also inhibiting tumor growth and KRAS expression in KRAS-mutant xenograft models. pan-KRAS-IN-5 is suitable for investigations into KRAS-related oncogenesis and therapeutic strategies for KRAS-driven cancers.
