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 -
two-site molecular glue
LL-K12-18 is a two-site molecular glue that enhances the protein-protein interaction between CDK12 and DDB1, stabilizing the complex and promoting cyclin K degradation with an EC50 of 0.37 nM. It exhibits potent transcriptional repression and anti-proliferative activity in tumor cells, making it a valuable tool for cancer research. -
FLT3/CHK2 inhibitor
Lasmotinib (PHI-101) is a dual inhibitor of FLT3 and CHK2 with potent activity against FLT3 single activating mutations (ITD or TKD), as well as double (ITD/D835Y or ITD/F691L) and triple (ITD/D835Y/F691L) resistance mutations. It synergizes with Venetoclax or Azacytidine to enhance anti-leukemic effects and also demonstrates anticancer activity in ovarian and breast cancer models. -
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. -
Aurora A/B inhibitor
Tinengotinib (TT00420) is an orally bioavailable, spectrally selective small-molecule kinase inhibitor targeting Aurora A/B (IC50=1.2–3.3 nM), FGFR1/2/3 (IC50=1.5–3.5 nM), VEGFRs, JAK1/2, and CSF1R. It disrupts Aurora kinase-mediated cell cycle progression, inducing G2/M arrest, inhibits the FGFR/JNK-JUN signaling pathway, and activates the MEK/ERK-dependent apoptotic pathway. Tinengotinib exhibits potent anti-tumor proliferation, pro-apoptotic, anti-angiogenic, and tumor microenvironment-modulating activities. It is a promising candidate for research in triple-negative breast cancer (TNBC), gallbladder cancer, and tumor immune microenvironment studies. -
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. -
Aurora B inhibitor
SP-96 is a highly potent, selective, and non-ATP-competitive inhibitor of Aurora B kinase, with an IC₅₀ of 0.316 nM. It exhibits exceptional selectivity, showing over 2000-fold greater specificity for Aurora B compared to off-target kinases such as FLT3 and KIT. In NCI-60 cancer cell line screening, SP-96 demonstrates selective antiproliferative activity, notably against the triple-negative breast cancer (TNBC) cell line MDA-MB-468 (GI₅₀ = 107 nM). SP-96 is a valuable tool for investigating Aurora B–driven oncogenic pathways and holds promise for the development of targeted therapies in TNBC and other malignancies. -
Aurora A inhibitor
CD532 is a potent Aurora A kinase (AURKA) inhibitor with an IC₅₀ of 45 nM. It exerts a dual mechanism of action by both inhibiting AURKA enzymatic activity and promoting the degradation of the MYCN oncoprotein. CD532 directly binds to AURKA and induces a global conformational shift, disrupting its functional interactions. This unique mode of action makes CD532 a valuable tool for cancer research, particularly in MYCN-amplified tumors such as neuroblastoma. -
Multi-target Inhibitor
Chiauranib (CS2164) is an orally active, multi-targeted small molecule inhibitor with potent anticancer activity. It targets key kinases involved in tumor angiogenesis, including VEGFR1, VEGFR2, VEGFR3, PDGFRα, and c-Kit, as well as mitosis-related kinase Aurora B and inflammation-associated kinase CSF-1R. Chiauranib exhibits IC₅₀ values ranging from 1 to 9 nM against these targets. Through simultaneous inhibition of angiogenesis, cell division, and inflammation pathways, Chiauranib exerts strong antitumor effects and is a promising candidate for the treatment of various solid tumors. -
Aurora A inhibitor
JAB-2485 is a highly potent and selective inhibitor of Aurora kinase A (AURKA), with an IC₅₀ of 0.33 nM. It exhibits exceptional selectivity, showing approximately 1700-fold preference for AURKA over Aurora kinase B (AURKB). JAB-2485 induces cell cycle arrest and apoptosis, making it a promising candidate for cancer research, particularly in tumors driven by dysregulated mitotic signaling. -
Aurora A inhibitor
Aurkin A is an allosteric inhibitor that disrupts the interaction between Aurora A kinase (AURKA) and its co-activator TPX2 by selectively targeting the TPX2 binding site on Aurora A. It binds with a dissociation constant (K\_d) of 3.77 μM, thereby interfering with Aurora A activation and its downstream mitotic functions. Aurkin A offers a unique mechanism of action compared to ATP-competitive inhibitors and serves as a valuable tool for studying Aurora A–TPX2–mediated signaling in cell division and cancer progression. -
Aurora A-TPX2 interaction inhibitor
CAM2602 is a selective inhibitor targeting the interaction between Aurora A kinase and its co-activator TPX2, with a high binding affinity of 19 nM for Aurora A. It effectively inhibits the growth of pancreatic cancer cells and demonstrates antitumor activity in solid tumor transplant models. Mechanistically, CAM2602 increases the proportion of phospho-histone H3 (PH3) positive cells—indicative of mitotic arrest—while decreasing the levels of Aurora A phosphorylated at threonine 288 (P-Thr288), a marker of Aurora A activation. These effects collectively contribute to its ability to disrupt mitosis and suppress tumor progression. -
Aurora kinase inhibitor
DBPR728 is an acyl prodrug of 6K465, engineered to improve pharmacokinetic properties by reducing the number of hydrogen bond donors, thereby enhancing membrane permeability and stability. As a prodrug of 6K465, DBPR728 functions as an Aurora kinase inhibitor that destabilizes MYC family oncoproteins, including c-MYC and N-MYC. It exhibits potent antitumor activity, particularly in cancers characterized by MYC overexpression. Notably, DBPR728 offers a 10-fold increase in oral bioavailability compared to 6K465, making it a promising candidate for the development of orally administered therapies targeting MYC-driven malignancies. - Phthalazinone pyrazole is a potent, selective, and orally bioavailable inhibitor of Aurora-A kinase, with an IC₅₀ of 0.031 μM. It exerts antitumor effects by arresting mitosis and inducing apoptosis in proliferating cells, leading to inhibition of tumor growth. Additionally, phthalazinone pyrazole suppresses epithelial-mesenchymal transition (EMT) during the differentiation of hepatocyte-like cells (HLCs) derived from human embryonic stem cells, indicating potential applications in both cancer therapy and stem cell biology.
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Aurora Kinase A/JAK2 Inhibitor
AJI-214 is a dual-target inhibitor that simultaneously inhibits Aurora kinase A and Janus kinase 2 (JAK2). It directly blocks Aurora A activity, disrupting T cell mitotic progression and polarity, while also inhibiting JAK2-mediated STAT3 phosphorylation, thereby suppressing the differentiation of pro-inflammatory TH1 and TH17 cells. AJI-214 holds therapeutic potential for modulating immune responses and is being investigated for the prevention and treatment of graft-versus-host disease (GVHD). -
Aurora A inhibitor.
6K465 is a pyrimidine-based small molecule inhibitor selectively targeting Aurora A kinase (AURKA). By inhibiting AURKA activity, 6K465 effectively reduces the expression levels of the oncogenic transcription factors c-MYC and N-MYC, contributing to its anticancer effects. This compound shows promise as a therapeutic agent for MYC-driven cancers by disrupting mitotic regulation and oncogene stabilization. -
Aurora kinase inhibitor
Derrone is a prenylated isoflavone that functions as an Aurora kinase inhibitor, exhibiting IC₅₀ values of 6 μM for Aurora B and 22.3 μM for Aurora A. By targeting these key mitotic kinases, Derrone disrupts cell cycle progression and displays notable antitumor activity, making it a promising compound for cancer research focused on mitotic regulation. - QW24 is a potent anti-tumor compound that exerts its effects by downregulating the expression of BMI-1, a key oncogenic regulator involved in cancer stem cell maintenance and tumor progression. It has demonstrated significant efficacy in preclinical models and is being explored as a promising therapeutic agent for clinical research in colorectal cancer.
- 1,6,7-Trihydroxyxanthone is a potent anticancer compound that inhibits tumor cell proliferation and induces apoptosis. It downregulates the expression of Bmi-1, a known oncogenic regulator, while upregulating the protein levels of tumor suppressors p14 and p16. These effects highlight its potential as a therapeutic agent for targeting oncogenic pathways in cancer research.
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Casein Kinase inhibitor
BTX-A51 (Casein Kinase Inhibitor A51) is a potent, orally bioavailable inhibitor of casein kinase 1α (CK1α). It effectively induces apoptosis in leukemia cells and demonstrates strong anti-leukemic activity in preclinical models, making it a promising therapeutic candidate for hematologic malignancies. -
PROTAC CDK12-Cyclin K degrader
PP-C8 is a potent and selective PROTAC degrader targeting the CDK12–Cyclin K complex. It induces efficient degradation of CDK12 and Cyclin K with DC₅₀ values of 416 nM and 412 nM, respectively. In preclinical models, PP-C8 exhibits strong synergistic antiproliferative effects when combined with PARP inhibitors, particularly in triple-negative breast cancer (TNBC), highlighting its potential as a therapeutic strategy for enhancing DNA damage response–targeted treatments. -
MYC-MAX degrader
MDEG-541 is a potent PROTAC degrader targeting the MYC-MAX complex, derived from the MYC-MAX dimerization inhibitor 10058-F4 (28RH) and thalidomide as the cereblon-recruiting ligand. It exhibits strong antiproliferative activity and reduces the expression of key oncogenic and regulatory proteins, including GSPT1, MYC, GSPT2, and PLK1. MDEG-541 is a valuable tool for studying MYC-driven cancers and targeted protein degradation strategies. -
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 CDK12/13 Degrader
PROTAC CDK12/13 Degrader-1 (7f) is a highly selective dual degrader targeting CDK12 and CDK13, with DC₅₀ values of 2.2 nM and 2.1 nM, respectively. It exhibits potent anti-proliferative activity and serves as a valuable tool for investigating transcriptional regulation and therapeutic strategies in breast cancer research. -
PROTAC Aurora A degrader
dAURK-4 hydrochloride is a potent and selective PROTAC degrader targeting Aurora A kinase (AURKA), derived from the AURKA inhibitor Alisertib. It effectively induces AURKA degradation and exhibits notable anticancer activity, making it a valuable agent for studying AURKA-driven oncogenic pathways and therapeutic development. -
PROTAC CDK8-cyclin C dual degrader
LL-K8-22 is a potent, selective, and durable PROTAC degrader targeting the CDK8–cyclin C complex, with DC₅₀ values of 2.52 μM and 2.64 μM, respectively. It suppresses STAT1 Ser727 phosphorylation and inhibits E2F- and MYC-driven oncogenic transcriptional programs. LL-K8-22 shows potential for use in triple-negative breast cancer (TNBC) research and related therapeutic studies. -
PROTAC CDK4/6 Degrader
XY028-133 (Example 14) is a PROTAC-based degrader targeting CDK4/6, composed of ligands for von Hippel-Lindau (VHL) and CDK. It induces selective degradation of CDK4/6 and exhibits anti-tumor activity, making it a useful tool for cell cycle and cancer research. -
PROTAC CDK4/6 Degrader
BSJ-03-204 triTFA is a potent and selective PROTAC degrader targeting CDK4/6, constructed using ligands for cereblon and CDK. Based on Palbociclib, it exhibits IC₅₀ values of 26.9 nM for CDK4/D1 and 10.4 nM for CDK6/D1. BSJ-03-204 triTFA does not induce IKZF1/3 degradation and shows anti-cancer activity, making it a valuable tool for cell cycle and oncology research. -
MYC RIBOTAC
MYC-RIBOTAC is a ribonuclease-targeting chimera (RIBOTAC) designed to degrade MYC mRNA by targeting its internal ribosome entry site (IRES). It combines a MYC mRNA-binding moiety with a small molecule that recruits and activates RNase L1. MYC-RIBOTAC reduces MYC mRNA and protein levels, induces apoptosis, and holds promise for antitumor research. -
PROTAC CDK12/13 Degrader
PROTAC CDK12/13 Degrader-1 (7f) TFA is a highly selective dual degrader of CDK12 and CDK13, with DC₅₀ values of 2.2 nM and 2.1 nM, respectively. It exhibits strong antiproliferative activity and is a valuable tool for investigating cell cycle regulation and therapeutic strategies in breast cancer research. -
PROTAC CDK12 Degrader
BSJ-4-116 is a PROTAC molecule derived from a modified form of the multi-kinase degrader TL12-186, linked to a cereblon ligand and E3 ligase ligand intermediate. It induces time- and concentration-dependent degradation of CDK12 in Jurkat T cells and downregulates genes involved in DNA double-strand break repair at 50 nM. BSJ-4-116 also inhibits MOLT-4 leukemia cell growth in a cereblon-dependent manner, supporting its application in cancer and DNA repair 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 CDK2/9 Degrader
PROTAC CDK2/9 Degrader-1 (Compound F3) is a potent dual PROTAC degrader targeting CDK2 (DC₅₀ = 62 nM) and CDK9 (DC₅₀ = 33 nM), constructed by linking a CDK inhibitor to a cereblon ligand. It effectively inhibits PC-3 prostate cancer cell proliferation (IC₅₀ = 0.12 µM) by inducing cell cycle arrest in the S and G2/M phases, making it a valuable tool for cancer and cell cycle 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. -
PROTAC CDK4 Degrader
BSJ-04-132 is a potent and selective Ribociclib-based PROTAC degrader targeting CDK4, constructed using ligands for cereblon and CDK. It exhibits IC₅₀ values of 50.6 nM for CDK4/D1 and 30 nM for CDK6/D1, while sparing CDK6 and IKZF1/3 from degradation. BSJ-04-132 demonstrates anti-cancer activity and is a valuable tool for cell cycle and oncology research. -
PROTAC CDK4/6 Degrader
BSJ-03-204 is a potent and selective PROTAC degrader targeting CDK4 and CDK6, constructed by linking Palbociclib to a cereblon ligand. It exhibits IC₅₀ values of 26.9 nM for CDK4/D1 and 10.4 nM for CDK6/D1, without inducing degradation of IKZF1 or IKZF3. BSJ-03-204 demonstrates strong anti-cancer activity and is a valuable tool for cell cycle and oncology research. -
multi-kinase PROTAC degrader
TL12-186 is a cereblon-dependent PROTAC degrader with broad-spectrum activity against multiple kinases, including CDKs, BTK, FLT3, Aurora kinases, TEC, ULK, and ITK. It inhibits CDK2/cyclin A and CDK9/cyclin T1 with IC₅₀ values of 73 nM and 55 nM, respectively, making it a valuable tool for studying kinase-driven signaling pathways and cancer biology. -
PROTAC CDK4/6 degrader
XY028-140 (MS140) is a highly potent and selective dual-function compound that acts as both a CDK4/6 kinase inhibitor and a PROTAC degrader. By combining kinase inhibition with targeted protein degradation, MS140 provides an effective approach for disrupting CDK4/6-mediated cell cycle regulation, making it a valuable tool for cancer research. -
CDK6-degrading PROTAC
YX-2-107 is a CDK6-degrading PROTAC with an IC50 of 4.4 nM, designed for selective degradation of CDK6. This compound effectively inhibits retinoblastoma (RB) phosphorylation and reduces FOXM1 expression in vitro. YX-2-107 has potential applications in research related to Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph+ ALL), demonstrating its ability to attenuate disease progression in rat models. -
CDK2 Degrader
CPS2 is a highly potent and selective PROTAC that irreversibly degrades cyclin-dependent kinase 2 (CDK2) with an IC50 of 24 nM. This compound is valuable for exploring the role of CDK2 in cell cycle regulation and has applications in the study of acute myeloid leukemia. Its unique mechanism provides a powerful tool for researchers investigating targeted protein degradation in cancer therapies. -
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 AURORA-A Degrader
JB170 is a potent PROTAC-mediated degrader targeting AURORA-A kinase, with a DC50 of 28 nM. By conjugating Alisertib with the Cereblon-binding molecule Thalidomide, JB170 selectively binds AURORA-A (EC50=193 nM) over AURORA-B (EC50=1.4 µM). The compound induces S-phase cell cycle arrest specifically via the depletion of AURORA-A and effectively inhibits its non-catalytic functions. JB170 serves as a valuable tool for studying AURORA-A's roles in cellular processes and therapeutic applications in cancer research. -
PROTAC CDK6 Degrader
CP-10 is a PROTAC designed to selectively target and degrade cyclin-dependent kinase 6 (CDK6) through its binding to Cereblon. Demonstrating a DC50 of 2.1 nM, this compound effectively inhibits the proliferation of various hematopoietic cancer cell lines, including multiple myeloma, and is capable of degrading both mutated and overexpressed forms of CDK6. Its specific activity makes CP-10 a valuable tool for research into CDK6-related malignancies and potential therapeutic strategies. -
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.
