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Catalog No.
Product Name
Application
Product Information
Citations
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CDK7 Inhibitor
SY-5609 (CDK7-IN-3) is an orally active, highly selective, and noncovalent inhibitor of CDK7, with a Kd of 0.065 nM. It demonstrates minimal activity against CDK2 (Ki = 2600 nM), CDK9 (Ki = 960 nM), and CDK12 (Ki = 870 nM), confirming its selectivity. SY-5609 induces apoptosis in tumor cells and exhibits potent antitumor activity, making it a promising candidate for targeted cancer therapy. -
CDK5 inhibitor
CP681301 is a potent CDK5 inhibitor with demonstrated antiproliferative activity. It reduces the expression of key stemness and proliferation markers—including CD133, OLIG2, SOX2, KI67, and phosphorylated CDK5—in glioma stem cells (GSCs). CP681301 also impairs self-renewal capacity in mouse glioma xenograft models and exhibits anti-tumor activity in *Drosophila*, making it a promising compound for glioma and cancer stem cell research. -
CDK2 inhibitor
INX-315 is an orally active and selective CDK2 inhibitor that induces G1 phase cell cycle arrest by reducing phosphorylation of CDK2 substrates. It exhibits dose-dependent tumor growth inhibition in xenograft mouse models and holds promise as a therapeutic candidate for cancer research targeting CDK2-driven malignancies. -
CDK8/19 inhibitor
Senexin B (SNX2-1-165; BCD-115) is a potent, highly water-soluble, and orally bioavailable inhibitor of CDK8 and CDK19, with Kd values of 140 nM for CDK8 and 80 nM for CDK19. It is a valuable tool for studying transcriptional regulation and has potential applications in cancer and inflammatory disease research. -
CDK2 inhibitor
Cirtociclib (BLU-222) is an orally active and highly selective CDK2 inhibitor. It disrupts retinoblastoma (Rb) signaling, leading to G1 cell cycle arrest and apoptosis, particularly in CCNE1-amplified endometrial cancer cells. Cirtociclib is a promising candidate for targeted therapy in CDK2-driven malignancies. -
CDK Inhibitor
Inixaciclib is a potent cyclin-dependent kinase (CDK) inhibitor with potential applications in anticancer research. By targeting CDKs involved in cell cycle regulation, Inixaciclib can inhibit tumor cell proliferation and is being explored as a therapeutic candidate in cancer treatment. -
CDK2 inhibitor
AZD8421 is a selective CDK2 inhibitor with an IC50 of 9 nM and demonstrated selectivity over CDK1, CDK4, and CDK6. It inhibits cancer cell proliferation by blocking pRB phosphorylation, leading to cell cycle arrest and senescence. AZD8421 shows strong single-agent efficacy and synergistic effects when combined with CDK4/6 inhibitors such as Palbociclib in in vivo models of breast and ovarian cancer. Additionally, it exhibits potent activity against drug-resistant breast cancer cells, making it a promising candidate for overcoming resistance in cancer therapy. -
DK/PI3K/BRD4 Inhibitor
SRX3177 is a potent triple inhibitor targeting CDK4/6, PI3K, and BRD4, with IC50 values of <2.5 nM for CDK4, 3.3 nM for CDK6, 79 nM for PI3Kα, 83 nM for PI3Kδ, 3.18 μM for PI3Kγ, and 33 nM and 89 nM for BRD4 BD1 and BD2, respectively. It exhibits broad cytotoxic activity against cancer cells while sparing normal epithelial cells, highlighting its potential as a targeted cancer therapeutic with reduced toxicity. -
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. -
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 -
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. -
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. -
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. -
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. -
CDK1 Inhibitor
Albanol B is a selective inhibitor of Cyclin-dependent kinase 1 (CDK1), derived from arylbenzofuran. This compound demonstrates significant potential in cancer research by inhibiting cell proliferation and down-regulating CDK1 expression, leading to G2/M cell cycle arrest and apoptosis in cancer cells. Additionally, Albanol B exhibits anti-Alzheimer's activity, antibacterial properties, and antioxidant effects, while also inducing mitochondrial reactive oxygen species (ROS) production and enhancing phosphorylation levels of AKT and ERK1/2. -
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. -
HDACs/CDKs Dual Inhibitor
CDK/HDAC-IN-3 is a dual inhibitor targeting histone deacetylases (HDACs) and cyclin-dependent kinases (CDKs). It exhibits potent and selective activity, with IC50 values of 98.32 nM, 98.85 nM, 100 nM, 62.12 nM, 93.28 nM, and 82.87 nM against CDK9, CDK12, CDK13, HDAC1, HDAC2, and HDAC3, respectively. This compound is particularly relevant for research in acute myeloid leukemia (AML), providing insights into therapeutic strategies for this disease. -
ROCK/NET Inhibitor
Netarsudil hydrochloride is a selective inhibitor of Rho-associated protein kinases (ROCK I and ROCK II) and a reversible inhibitor of the norepinephrine transporter (NET). It effectively lowers intraocular pressure by promoting relaxation of trabecular meshwork cells and dilation of episcleral veins, enhancing aqueous humor outflow while simultaneously reducing its production. This compound is primarily utilized in research related to ocular hypertension and primary open-angle glaucoma. -
Chk-α Inhibitor
V-11-0711 is a potent and selective inhibitor of Chk-α, exhibiting an IC50 value of 20 nM. This compound effectively reduces phosphocholine (PCho) levels and induces reversible growth arrest in various cancer cell lines. At elevated concentrations, V-11-0711 can promote apoptosis. It is particularly useful for research related to cervical cancer and triple-negative breast cancer, facilitating the exploration of therapeutic strategies targeting Chk-α pathways. -
CDK6/PIM1 Inhibitor
CDK6/PIM1-IN-1 hydrochloride is a potent dual inhibitor targeting CDK6 and PIM1, exhibiting IC50 values of 39 nM and 88 nM, respectively, along with significant inhibition of CDK4 (IC50=3.6 nM). This compound effectively inhibits the proliferation of acute myeloid leukemia (AML) cells, induces G1 phase cell cycle arrest, and promotes apoptosis. CDK6/PIM1-IN-1 hydrochloride is a valuable tool for research investigating the role of CDK6 and PIM1 in cancer biology, particularly in the context of AML. -
Wee1 Inhibitor
WEE1-IN-7 is a selective Wee1 inhibitor with an IC50 value of 2.1 nM. This compound induces apoptosis and facilitates cell cycle arrest during the S phase, making it valuable in the study of tumor biology. WEE1-IN-7 demonstrates significant antitumor activity, providing a useful tool for cancer research and therapeutic development. -
PLK1 Inhibitor
Volasertib trihydrochloride is a potent, ATP-competitive inhibitor of Polo-like kinase 1 (PLK1) with an IC50 of 0.87 nM. This compound also exhibits inhibitory activity against PLK2 and PLK3 with IC50s of 5 nM and 56 nM, respectively. Volasertib trihydrochloride induces mitotic arrest and apoptosis in cancer cells, demonstrating significant antitumor efficacy across various cancer models. It is a valuable tool for research focused on cell division and the development of cancer therapeutics. -
cyclin D1 Inhibitor
Dehydrozingerone is a cyclin D1 inhibitor derived from ginger, known for its ability to downregulate cyclin D1 expression and induce G1 phase cell cycle arrest. This compound effectively reduces the proliferative capacity of castration-resistant prostate cancer cells in vitro and inhibits subcutaneous tumor growth by targeting cell proliferation and angiogenesis. Additionally, dehydrozingerone demonstrates notable antibacterial and antifungal properties, making it suitable for research into castration-resistant prostate cancer, bacterial infections, and food spoilage due to fungal infections. -
cyclin D1/CDK4 Inhibitor
Arcyriaflavin A is an indolo[2,3-a]carbazole compound that primarily acts as a cyclin D1/CDK4 inhibitor. This compound, derived from the marine ascidian Eudistoma sp. and the slime mold Arcyria denudata, demonstrates significant biological activity in regulating the cell cycle. Arcyriaflavin A is particularly relevant for research applications focusing on colon and lung cancer, providing insights into tumor growth and potential therapeutic strategies. -
EGFR/HER2/CDK9 Inhibitor
EGFR/HER2/CDK9-IN-2 is a potent inhibitor targeting EGFR, HER2, and CDK9, exhibiting IC50 values of 145.35 nM, 129.07 nM, and 117.13 nM, respectively. This compound demonstrates significant antitumor activity, making it a valuable tool for cancer research. Its ability to concurrently inhibit these kinases positions it as a promising candidate for studies focused on targeted therapy and oncogenic signaling pathways. -
DYRK1A Inhibitor
Dyrk1A-IN-16 is a selective DYRK1A inhibitor that operates as an ATP-competitive antagonist with an IC50 of 53 nM. This compound exhibits strong selectivity for DYRK kinases and demonstrates nanomolar potency in biological assays. In vitro studies reveal that Dyrk1A-IN-16 effectively impairs neurosphere self-renewal, cell invasion, and EGFR stability. In vivo, it has been shown to inhibit tumor growth and extend survival, indicating its potential utility in glioblastoma research. -
EGFR/HER2/CDK9/COX-2 Inhibitor
CDK9-IN-41 is a potent inhibitor of CDK9, EGFR, HER2, and COX-2, exhibiting IC50 values of 192.81 nM, 254.03 nM, 238.81 nM, and 775 nM respectively. This compound demonstrates significant antitumor activity across various cancer cell lines, including leukemia, colon, melanoma, ovarian, and breast cancer. It serves as a valuable tool for exploring the role of these kinases in cancer biology and therapeutic applications. -
EGFR/HER2/CDK9 Inhibitor
EGFR/HER2/CDK9-IN-3 is a potent inhibitor targeting EGFR, HER2, and CDK9, exhibiting IC50 values of 191.08 nM, 132.65 nM, and 113.98 nM, respectively. This compound demonstrates significant antitumor activity, making it valuable for research in cancer therapies and signaling pathways involving these targets. Its inhibitory effects on cell proliferation in cancer models may aid in the understanding and development of targeted treatment strategies. -
EGFR/HER2/CDK9 Inhibitor
EGFR/HER2/CDK9-IN-1 is a highly active inhibitor of EGFR, HER2, and CDK9, displaying IC50 values of 90.17 nM, 131.39 nM, and 67.04 nM, respectively. This compound demonstrates significant antitumor properties, making it a valuable tool for cancer research. Its ability to target multiple kinases involved in cell proliferation and survival pathways supports investigations into therapeutic strategies for various malignancies. -
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. -
DYRK1A Inhibitor
Dyrk1A-IN-15 is a selective, ATP-competitive inhibitor of DYRK1A with an IC50 of 19 nM. This compound demonstrates high selectivity for DYRK kinases and nanomolar potency across various kinase assays. In vitro studies reveal that Dyrk1A-IN-15 disrupts neurosphere self-renewal, inhibits cell invasion, and destabilizes EGFR. Additionally, it shows the ability to inhibit tumor growth and extend survival in vivo, indicating its potential utility in glioblastoma research.
