Catalog No.
Product Name
Application
Product Information
Citations
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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. -
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. -
KRAS Inhibitor
KRAS G12D inhibitor 25 selectively targets the KRAS G12D mutation and HSP90α, exhibiting IC50 values of less than 0.1 μM and between 0.1-1 μM, respectively. This compound effectively inhibits the proliferation of MIA PaCa-2 and NCI-H358 cell lines, displaying EC50 values of less than 0.1 μM and between 0.1-1 μM, respectively. Additionally, KRAS G12D inhibitor 25 promotes the degradation of ERBB2 with a DC50 range of 0.1-1 μM, making it a valuable tool for cancer research focusing on KRAS-targeted therapies. -
KRASG12C Inhibitor
KRASG12C IN-19 is a selective inhibitor that targets the KRASG12C mutation. It demonstrates potent antiproliferative effects against KRASG12C-mutant non-small cell lung cancer (NSCLC) cell line H358, with an IC50 of 7.6 nM, and effectively inhibits downstream ERK phosphorylation (IC50 = 24.06 nM). KRASG12C IN-19 shows minimal inhibitory activity against KRASG12V and KRASG12D mutants, with IC50 values exceeding 10,000 nM. This reagent forms a covalent bond with KRASG12V-GDP and provides a robust tool for research on KRASG12C-driven malignancies, including NSCLC, pancreatic cancer, and colorectal cancer. -
RAS/RAS-RAF Inhibitor
RAS/RAS-RAF-IN-1 is a potent inhibitor targeting the RAS and RAS-RAF signaling pathways. With a dissociation constant (KD) in the range of 5.0 μM to 15 μM for cyclophilin A (CYPA), this compound demonstrates significant binding affinity. RAS/RAS-RAF-IN-1 exhibits notable antitumor activity, making it a valuable tool for cancer research and therapeutic development. -
Ras-Raf Inhibitor
Cyclorasin 9A5 is an 11-residue cyclic peptide that acts as an orthosteric inhibitor of the Ras-Raf protein interaction, exhibiting an IC50 of 120 nM. This compound is valuable for studying the Ras signaling pathway's involvement in various cancers and cellular processes. Its cell-permeable nature allows for effective in vitro and in vivo applications in cancer research and drug development targeting Ras-dependent pathways. -
pan-KRAS PROTAC Degrader
MCB-36 is a VHL-recruiting pan-KRAS PROTAC degrader that targets various KRAS mutants, including G12D, G12C, G12V, and wild-type forms, with an exceptionally high binding affinity (Kd ≈ 1 pM). This compound effectively lowers p-ERK levels, promoting apoptosis in KRAS-driven cancer cells while showing minimal impact on HRAS and NRAS protein levels. MCB-36 is particularly useful for investigating colorectal and lung cancers, as it demonstrates efficacy against KRASG12C inhibitor-resistant tumors and aids in remodeling the tumor immune microenvironment. -
PDE6δ-KRas Inhibitor
Deltasonamide 1 is a potent inhibitor of the PDE6δ-KRas interaction, exhibiting a dissociation constant (KD) of 203 pM. This compound effectively disrupts the function of the KRas signaling pathway, making it a valuable tool for investigating tumor biology and related therapeutic strategies. Deltasonamide 1 holds promise for advancing research in cancer treatment and understanding related pathophysiological mechanisms. -
KRAS Inhibitor
Deltarasin hydrochloride is a potent inhibitor of the interaction between KRAS and PDEδ, exhibiting a binding affinity (Kd) of 38 nM for purified PDEδ. This compound is crucial for research applications focused on targeting KRAS-driven oncogenesis, primarily in cancer studies. By disrupting this interaction, Deltarasin hydrochloride facilitates investigations into therapeutic strategies aimed at KRAS mutations and their downstream signaling pathways. -
PDE6δ-KRas Inhibitor
Deltasonamide 1 TFA is a potent inhibitor of the PDE6δ-KRas interaction, exhibiting a binding affinity with a KD of 203 pM. This compound is valuable in research focused on cancer biology, particularly in the study of tumor progression and metastasis. Its ability to disrupt the PDE6δ-KRas axis makes it a useful tool for investigating the underlying mechanisms of KRas-driven malignancies. -
KRAS G12C Inhibitor
KRAS G12C-IN-78 is a selective inhibitor targeting the KRAS G12C mutant protein, binding to both inactive and active states. This compound effectively inhibits ERK1/2 phosphorylation and promotes covalent adduct formation with endogenous KRAS G12C, leading to the suppression of MAPK pathway gene expression and reduced cellular proliferation in KRAS G12C mutant cells. KRAS G12C-IN-78 is suitable for studying KRAS G12C mutant solid tumors, such as pancreatic ductal adenocarcinoma and non-small cell lung cancer. -
KRAS-PDEδ Inhibitor
NHTD is a selective inhibitor of KRAS-PDEδ, targeting the prenyl-binding pocket of PDEδ and modulating the cellular localization of KRAS. This action effectively inhibits the proliferation of KRAS-mutant cancer cells and promotes apoptosis. NHTD is a valuable tool for investigations into KRAS-driven non-small cell lung cancer (NSCLC) and related oncology research. -
KRAS Inhibitor
KRAS-IN-56 is a selective KRAS inhibitor that targets the interaction between GTP-bound KRAS and SOS1, demonstrating an EC50 of 33 μM. This compound effectively reduces phosphorylated ERK (p-ERK) levels, making it a valuable tool for studying MAPK signaling pathways. KRAS-IN-56 is particularly relevant for research applications involving lung cancer and other KRAS-driven malignancies. -
pan-KRAS Inhibitor
Eras-4001 is a pan-KRAS inhibitor that demonstrates significant antitumor activity by effectively inhibiting the proliferation of both wild-type and mutant KRAS cancer cells, including variants such as KRASG12D, KRASG12V, and KRASG12C. In preclinical studies, Eras-4001 has evidenced a robust ability to suppress tumor growth in xenograft mouse models, such as GP2D and Panc0403, making it a valuable tool for investigating KRAS-driven malignancies and potential therapeutic strategies in cancer research. -
KRAS Agonist
KRA-533 is a potent KRAS agonist that selectively binds to the GTP/GDP binding pocket of the KRAS protein. This interaction inhibits GTP cleavage, leading to the accumulation of constitutively active GTP-bound KRAS. Consequently, KRA-533 induces both apoptotic and autophagic cell death pathways in cancer cells, making it a valuable tool for research into cancer biology and therapeutic strategies targeting KRAS signaling. -
Cdc42 Inhibitor
CID44216842 is a selective inhibitor of the small GTPase Cdc42, acting primarily by disrupting its guanine nucleotide binding. It demonstrates potent inhibitory activity with EC50 values of 1.0 μM and 1.2 μM for wild-type Cdc42 and the Cdc42Q61L mutant, respectively, in GTP binding assays, and 0.3 μM and 0.5 μM in GDP binding assays. This compound is suitable for use as a molecular probe in studies related to Cdc42 signaling pathways and its role in cellular processes such as cytoskeletal dynamics and cell migration. -
KRAS G12D Inhibitor
AZD0022 is a selective and orally active inhibitor of the KRAS G12D mutant protein. It effectively disrupts the KRAS signaling pathway, demonstrating suppression of tumor growth in the GP2D xenograft model. This compound is relevant for research in cancer therapeutics, particularly for investigating KRAS-driven malignancies. -
KRAS Inhibitor
KRAS inhibitor-3 is a selective inhibitor of the KRAS protein, effectively targeting both wild-type and various oncogenic mutants, including KRAS G12C, G12D, and Q61H, with affinities ranging from 0.28 μM to 0.74 μM. This compound disrupts the interaction between KRAS and Raf, thereby influencing downstream signaling pathways critical for cell proliferation and survival. KRAS inhibitor-3 is a valuable tool for research applications focused on cancer biology and the development of targeted therapies for KRAS-driven malignancies. -
Cdc42/Rac1 Inhibitor
l-Naproxen is an enantiomer of (S)-Naproxen, functioning as an inhibitor of Cdc42 and Rac1 with EC50 values of 96 μM and 212 μM, respectively. It exhibits anti-tumor activity in addition to its role as a nonsteroidal anti-inflammatory drug (NSAID). This compound is valuable for research applications involving cellular signaling pathways, inflammation, and cancer biology. -
KRasG12C Inhibitor
CFL-137 is a potent inhibitor of KRasG12C, a pivotal mutation implicated in various cancers. This compound demonstrates significant antiproliferative activity, making it a valuable tool for studying oncogenic signaling pathways. CFL-137 holds promise for research applications focused on lung cancer and other KRas-driven malignancies. -
KRAS Inhibitor
KRAS Inhibitor-10 is a selective inhibitor targeting RAS proteins, with a strong emphasis on KRAS variants. This orally active compound demonstrates significant anti-cancer activity, making it suitable for research applications in various malignancies, including pancreatic cancer, breast cancer, multiple myeloma, leukemia, and lung cancer. KRAS Inhibitor-10 is derived from a tetrahydroisoquinoline structure and is detailed in patent WO2021005165 A1. -
KRASG12D Mutant Inhibitor
KRAS G12D-IN-29 is a selective inhibitor targeting the KRAS G12D mutant, known for its oral bioavailability. This compound effectively disrupts downstream signaling pathways associated with KRAS G12D, leading to a reduction in tumor cell proliferation. KRAS G12D-IN-29 shows potential for research applications focused on cancers driven by the KRAS G12D mutation, including pancreatic, lung, and colorectal cancers. -
KRAS Inhibitor
KRAS Inhibitor-31 is a potent inhibitor targeting mutant forms of the KRAS protein, specifically KRAS G12D, G12C, and G12V, with KD (SPR) values of 0.019 nM, 0.019 nM, and 0.096 nM, respectively. This compound demonstrates significant biological activity in the inhibition of KRAS-driven signaling pathways, making it a valuable tool for research in cancer biology, particularly in the study of tumors harboring KRAS mutations. -
pan-KRAS Inhibitor
pan-KRAS-IN-2 is a potent pan-KRAS inhibitor with IC50 values of ≤ 10 nM against both wild-type and prevalent mutant forms of KRAS, including G12D, G12C, G12V, G12S, G12A, and Q61H, while exhibiting an IC50 > 10 μM for KRAS G13D. This compound is valuable for investigating KRAS-mediated cancers, specifically in pancreatic and colorectal cancer models, aiding in the understanding of tumor biology and potential therapeutic interventions. -
EPAC1 Agonist
I942 is a selective non-cyclic nucleotide (NCN) agonist of EPAC1. It effectively modulates proinflammatory cytokine signaling pathways associated with various cardiovascular diseases. This compound serves as a valuable tool in research focused on understanding EPAC1-related mechanisms and developing therapeutic strategies for inflammatory cardiovascular conditions. -
Isomer
(R)-BI-2852 is the isomer of BI-2852, designed as an experimental control in KRAS research. It functions as a KRAS inhibitor targeting the switch I/II pocket with nanomolar affinity, displaying a ten-fold stronger binding to active KRASG12D compared to KRAS wild type. This compound effectively disrupts guanine nucleotide exchange factor, GTPase-activating protein, and effector interactions with KRAS, resulting in the inhibition of downstream signaling pathways and an antiproliferative effect in KRAS mutant cell lines. -
Rac1 Inhibitor
Rac1-IN-3 is an inhibitor of the Rac1 protein, exhibiting an IC50 of 46.1 μM. This compound effectively disrupts Rac1 signaling pathways, which are implicated in various cellular functions such as cytoskeletal dynamics and cell migration. Rac1-IN-3 is valuable for research applications focused on cancer biology, neurodegenerative diseases, and cardiovascular disorders, providing insights into the role of Rac1 in disease progression and therapeutic targeting. -
pan-KRAS Inhibitor
pan-KRAS-IN-18 is a pan-KRAS inhibitor targeting both KRAS wild-type and KRAS G12V, with IC50 values of 29 nM and 9 nM, respectively. This compound demonstrates significant antiproliferative activity in KRAS-mutant cell lines, making it a valuable tool for researchers studying KRAS-driven cancers. Its application is particularly relevant in the context of lung cancer research. -
KRAS G12C Inhibitor
Divarasib adipate is a potent and selective inhibitor of KRAS G12C with an IC50 of <0.01 μM. By covalently binding to the switch II pocket of KRAS G12C, Divarasib irreversibly stabilizes the protein in its inactive GDP-bound state. This compound is primarily utilized in research applications focused on cancer biology, particularly in studies targeting KRAS-driven tumors. -
KRAS(G12D) Inhibitor
MRTX-EX185 formic is a potent inhibitor of KRAS(G12D) with an IC50 of 90 nM. It effectively binds to both GDP-loaded and active GTP-bound states of KRAS, displaying broad-spectrum activity with additional IC50 values of 110, 290, 130, and 240 nM for KRAS WT, KRAS(G12C), KRAS(Q61H), and KRAS(G13D), respectively. MRTX-EX185 formic also shows affinity for GDP-loaded HRAS. This compound is valuable for investigating RAS-driven tumors, including pancreatic cancer, facilitating insights into therapeutic strategies targeting KRAS mutations. -
Pan-RAS Inhibitor
Pan-RAS-IN-3 is a pan-RAS inhibitor that targets various isoforms of the RAS protein family, known for their role in promoting cellular proliferation and survival. This compound exhibits significant biological activity in inhibiting the signaling pathways associated with melanoma and acute myeloid leukemia. It is a valuable tool for researchers investigating RAS-driven cancers and studying the therapeutic potential of targeting these oncogenic signaling pathways. -
KRAS Inhibitor
KRAS inhibitor-24 is a pyridopyrimidine compound that selectively inhibits KRAS with an IC50 of less than 100 nM for KRas G12V, KRas WT, and KRas G12R mutants. This compound demonstrates substantial biological activity in disrupting KRAS-mediated signaling pathways. KRAS inhibitor-24 is utilized in preclinical research to study KRAS-driven tumors and to investigate potential therapeutic strategies targeting KRAS mutations in various cancers. -
KRAS Inhibitor
(1R)-KRAS inhibitor-24 is a pyridopyrimidine compound that selectively inhibits KRAS, demonstrating an IC50 of less than 100 nM for KRas G12V, KRas Wild Type, and KRas G12R variants. This inhibitor serves as a valuable tool for research applications focused on KRAS-driven cancers, providing insights into signaling pathways and potential therapeutic modalities targeting this critical oncogene. -
KRAS G12D Inhibitor
KRAS G12D-IN-31 is a potent inhibitor of the KRAS G12D mutation, exhibiting an IC50 of less than 100 nM. It effectively inhibits the proliferation of RAS-dependent cancer cells, including those harboring KRAS G12C, KRAS G12D, KRAS G12V, and KRASWT. This compound is particularly valuable for research applications involving non-small cell lung cancer, gastric cancer, colon cancer, and malignant melanoma, facilitating the exploration of KRAS-targeted therapies. -
RAS Ligand
VVD-849 is a RAS ligand that covalently binds to Cys242 in the RAS-binding domain of PI3K p110α, facilitating the interaction between RAS and PI3K. This compound exhibits partial inhibition of pAKT (S473) specifically in HER2-overexpressing tumors. VVD-849 is utilized in cancer research, particularly for studying the mechanisms underlying breast cancer progression and RAS-related signaling pathways. -
KRAS(G12D) Inhibitor
TH-Z827 is a selective inhibitor of the KRAS(G12D) mutant, demonstrating an IC50 of 2.4 μM. This compound does not interact with wild-type KRAS or the KRAS(G12C) variant. TH-Z827 effectively disrupts the interaction between KRAS(G12D) and CRAF, with an IC50 value of 42 μM, making it a valuable tool for studying KRAS-driven cancers and developing targeted therapies. -
KRAS G12D Inhibitor
KRAS G12D Inhibitor 3 TFA is a selective inhibitor targeting the KRAS G12D mutation, exhibiting an IC50 of less than 500 nM. This compound demonstrates significant antitumor activity, making it a valuable tool in cancer research related to KRAS-driven malignancies. Additionally, KRAS G12D Inhibitor 3 TFA features an alkyne functional group, enabling it to participate in copper-catalyzed azide-alkyne cycloaddition (CuAAc), thus facilitating the development of bioconjugates and other applications in chemical biology. -
Lbc-RhoA Interaction Inhibitor
(E/Z)-ZINC09659342 is a potent inhibitor of the Lbc-RhoA protein interaction, impacting RhoA-mediated cellular signaling pathways. This compound is valuable for studies focused on RhoA's role in cell adhesion, migration, and cytoskeletal dynamics. It serves as a useful tool for researchers investigating the molecular mechanisms of various diseases associated with RhoA dysregulation. -
KRAS G12C Inhibitor
KRAS G12C inhibitor 14 is a potent inhibitor specifically targeting the KRAS G12C mutation, with an IC50 value of 18 nM. This compound effectively disrupts the activity of the KRAS protein, making it a valuable tool for studies on cancer biology, particularly in models of tumors driven by KRAS mutations. Its application extends to drug discovery and development efforts aimed at novel therapeutic strategies for KRAS-driven malignancies. -
ADT-007 Prodrug
ADT-1004 is an orally active prodrug of the pan-RAS inhibitor ADT-007, which is characterized by its reversible, high potency and selectivity. By binding to the nucleotide-free conformation of RAS proteins, ADT-007 effectively inhibits GTP activation, subsequently blocking downstream MAPK and AKT signaling pathways. ADT-1004 is primarily utilized in research focused on pancreatic ductal adenocarcinoma, providing a valuable tool for the investigation of RAS-mediated oncogenic processes.
