Catalog No.
Product Name
Application
Product Information
Citations
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CDK Inhibitor
3-Methylthienyl-carbonyl-JNJ-7706621 is a selective cyclin-dependent kinase (CDK) inhibitor, demonstrating potent activity with IC50 values of 6.4 nM for CDK1/cyclin B and 2 nM for CDK2/cyclin A. Additionally, it exhibits strong inhibition of GSK-3 (IC50=0.041 μM) and moderate inhibition against CDK4, VEGF-R2, and FGF-R2 with IC50s of 0.11, 0.13, and 0.22 μM, respectively. This compound is primarily utilized in cancer research to explore CDK-related pathways and therapeutic strategies. -
CDK1/Cyc B Inhibitor
CDK1/Cyc B-IN-1 is a selective inhibitor of the CDK1/cyclin B complex, demonstrating an IC50 of 97 nM. This compound effectively induces apoptosis and facilitates G2/M phase cell cycle arrest, making it a valuable tool for studying cell proliferation. CDK1/Cyc B-IN-1 exhibits broad-spectrum cytotoxic activity against various cancer cell lines, supporting its potential in cancer research applications. -
CDK/CRK Inhibitor
RGB-286147 is a selective ATP-competitive inhibitor of cyclin-dependent kinases (CDKs) and CDK-related kinases (CRKs), exhibiting IC50 values between 9 to 839 nM. This compound demonstrates minimal activity against non-CDK/CRK kinases. RGB-286147 induces apoptosis in cancer cells and shows significant anti-tumor effects, making it a valuable tool for research in cancer biology and therapeutic development targeting CDK pathways. -
CDK4/6 Degrader
LA-CB1 is a CDK4/6 degrader that promotes the degradation of cyclin-dependent kinases 4 and 6 through the ubiquitin-proteasome pathway. This action disrupts the CDK4/6-Cyclin D1-Rb-E2F signaling axis, leading to G0/G1 cell cycle arrest and apoptosis. LA-CB1 demonstrates potent anti-proliferative effects against MDA-MB-231 cells, with an IC50 of 0.27 µM, and effectively inhibits epithelial-mesenchymal transition, cell migration, invasion, and angiogenesis. In models of triple-negative breast cancer, LA-CB1 significantly inhibits tumor growth in a dose-dependent manner, making it a valuable compound for research in breast cancer therapeutics. -
CHK1 Inhibitor
Prexasertib Mesylate Hydrate is a selective, ATP-competitive inhibitor of checkpoint kinase 1 (CHK1) with a Ki of 0.9 nM and an IC50 of <1 nM. It also inhibits checkpoint kinase 2 (CHK2) with an IC50 of 8 nM and ribosomal S6 kinase 1 (RSK1) with an IC50 of 9 nM. By inducing double-stranded DNA breakage and replication catastrophe, Prexasertib Mesylate Hydrate promotes apoptotic cell death, exhibiting significant anti-tumor activity. This reagent is primarily utilized in cancer research to explore mechanisms of DNA damage response and therapeutic resistance. -
c-MYC Inhibitor
IZTZ-1 is an imidazole-benzothiazole conjugate that functions as a c-MYC inhibitor by stabilizing the G-quadruplex (G4) structure of c-MYC. This stabilization results in the downregulation of c-MYC expression, leading to induction of cell cycle arrest and apoptosis in various cell lines, including B16 melanoma cells. Due to its ability to inhibit cell proliferation and exhibit antitumor activity, IZTZ-1 is a valuable tool for researchers studying melanoma and related cancer pathways. -
ROCK Inhibitor
PT-262 is a selective ROCK inhibitor with an IC50 of approximately 5 μM. This compound induces loss of mitochondrial membrane potential and enhances caspase-3 activation, leading to apoptosis. PT-262 also inhibits phosphorylation of ERK and CDC2 through a p53-independent mechanism, disrupts cytoskeletal dynamics, and impairs cell migration. Its efficacy in promoting anti-cancer activity makes PT-262 a valuable reagent for cancer research. -
Aurora kinase Inhibitor
Aurora kinase-IN-8 is an orally active inhibitor of Aurora kinases, specifically targeting Aurora A and B kinases with IC50 values of 2.8 nM and 28.1 nM, respectively. This compound effectively disrupts spindle formation, induces G2/M phase arrest, and promotes apoptosis in cancer cells. It is particularly relevant for research applications focused on malignancies, including triple-negative breast cancer. -
CDK6/PIM1 Inhibitor
CDK6/PIM1-IN-1 is a potent dual inhibitor targeting CDK6 and PIM1, with IC50 values of 39 nM and 88 nM, respectively, and an additional inhibition of CDK4 at an IC50 of 3.6 nM. This reagent significantly inhibits the proliferation of acute myeloid leukemia (AML) cells, induces G1 phase cell cycle arrest, and promotes apoptosis. CDK6/PIM1-IN-1 demonstrates strong anti-AML activity, making it a valuable tool for research in cancer biology and therapeutic development. -
CDK Inhibitor
1-Stearoyl-2-Adrenoyl-sn-glycero-3-PC is a cyclin-dependent kinase (CDK) inhibitor that plays a crucial role in cancer research. This compound induces apoptosis and effectively inhibits the proliferation of a variety of cancer cell lines, making it a valuable tool for studying cancer biology and therapeutic responses. Its ability to impact CDK activity provides insights into cell cycle regulation and potential cancer treatment strategies. -
Aurora A Kinase Inhibitor
Alisertib sodium is a selective inhibitor of Aurora A kinase, exhibiting an IC50 of 1.2 nM. This compound disrupts mitotic spindle formation and leads to mitotic accumulation, thereby inducing apoptosis and autophagy in leukemic cells via the AKT/mTOR/AMPK/p38 signaling pathway. Alisertib sodium demonstrates significant antitumor activity, making it a valuable reagent for cancer research and therapeutic applications. -
CHK1 Inhibitor
Prexasertib mesylate is a selective ATP-competitive inhibitor of checkpoint kinase 1 (CHK1), demonstrating a Ki of 0.9 nM and an IC50 of less than 1 nM. It also inhibits CHK2 and RSK1 with IC50 values of 8 nM and 9 nM, respectively. By inducing double-stranded DNA breaks and triggering replication catastrophe, Prexasertib mesylate leads to apoptosis. Its potent anti-tumor activity makes it valuable for cancer research applications, particularly in studies focusing on DNA damage response and cell cycle regulation. -
Selective ROCK Inhibitor
Y-27632 hydrochloride hydrate is a selective inhibitor of Rho-associated protein kinases (ROCK-I and ROCK-II), exhibiting ATP-competitive activity with IC50 values of 220 nM and 300 nM, respectively. This compound has been shown to reduce Doxorubicin-induced apoptosis in human cardiac stem cells and suppress apoptosis in dissociation-induced murine prostate stem/progenitor cells. Additionally, Y-27632 hydrochloride hydrate enhances the differentiation of human induced pluripotent stem cells (hIPSCs) towards a mesendodermal lineage by modulating epithelial-mesenchymal transition. -
HDAC1/2 and CDK2 Inhibitor
HDAC1/2 and CDK2-IN-1 is a dual inhibitor targeting HDAC1, HDAC2, and CDK2, with IC50 values of 70.7 μM, 23.1 μM, and 0.80 μM, respectively. This compound effectively disrupts the cell cycle and promotes apoptosis in tumor cells, demonstrating significant in vivo antitumor activity. It is suitable for research applications focused on cancer biology and therapeutic interventions targeting histone deacetylases and cyclin-dependent kinases. -
CDK2/9 Inhibitor
ZLMT-12 is a potent CDK2/9 inhibitor, demonstrating IC50 values of 0.002 μM and 0.011 μM against CDK9 and CDK2, respectively. This compound is derived from tacrine and exhibits weak inhibition of acetylcholinesterase (IC50 = 19.023 μM) and butyrylcholinesterase (IC50 = 2.768 μM). ZLMT-12 is characterized by low toxicity and notable antiproliferative activity, effectively inducing apoptosis and facilitating cell cycle arrest in the S and G2/M phases. This compound serves as a valuable tool for research in cell cycle regulation and therapeutic development in cancer biology. -
Aurora B Inhibitor
Barasertib dihydrochloride is a selective inhibitor of Aurora B kinase, exhibiting an IC50 of 0.37 nM in cell-free assays. This compound effectively induces growth arrest and apoptosis in various cancer cell lines, making it a valuable tool for cancer research. Its mechanism of action provides insights into the role of Aurora B in cell cycle regulation and tumorigenesis. -
Aurora/JAK Inhibitor
AT9283 lactic acid is a multi-targeted kinase inhibitor primarily targeting Aurora A/B and JAK2/3. It demonstrates potent biological activity against various cancers, exhibiting IC50 values between 1 to 30 nM for its targets. AT9283 lactic acid effectively inhibits the growth and survival of multiple solid tumors in both in vitro and in vivo models, making it a valuable reagent for cancer research applications. -
CDK7 Inhibitor
CDK7-IN-30 is a potent CDK7 inhibitor with an IC50 value of 7.21 nM, targeting the phosphorylation of RNA Polymerase II and CDK2. This compound demonstrates significant pro-apoptotic effects and exhibits anti-cancer activity, making it a valuable tool for cancer research. Its mechanism of action offers insights into cell cycle regulation and transcriptomic processes, facilitating the exploration of therapeutic strategies in oncology. -
CDK9 Inhibitor
A-1592668 is a selective inhibitor of cyclin-dependent kinase 9 (CDK9), which plays a critical role in transcriptional regulation. This compound induces apoptosis in various cancer cell lines and demonstrates synergistic effects when combined with Venetoclax, effectively inhibiting the growth of Jeko-1 tumors. A-1592668 is a valuable tool for research in cancer biology and therapeutic development targeting CDK9 pathways. -
CDK6/BRD4 Inhibitor
BC13 is a selective inhibitor of CDK6 and BRD4, demonstrating IC50 values of 234 nM and 36 nM, respectively. This compound exhibits notable antiproliferative effects, facilitating cell apoptosis and inducing DNA damage in various cell lines. Additionally, BC13 has been shown to elevate reactive oxygen species (ROS) levels, making it a valuable tool for research in cancer biology and therapeutic development targeting cell cycle regulation. -
Aurora A/Aurora B/HDAC1/HDAC2 Inhibitor
Aurora kinase/HDAC-IN-1 is a potent dual inhibitor targeting Aurora A, Aurora B, HDAC1, and HDAC2. This compound promotes histone H3 acetylation, inhibits Aurora A phosphorylation and downstream signaling, and induces apoptosis through G2/M cell-cycle arrest. It demonstrates significant antiproliferative activity in colorectal cancer cells, with an IC50 of 30.2 nM in HCT-116 cells, and effectively suppresses tumor growth in HCT-116 colorectal cancer xenograft mouse models. This reagent is valuable for research in cancer biology and therapeutic application development. -
HDAC1/CDK7 Inhibitor
HDAC1/CDK7-IN-1 is a dual inhibitor targeting HDAC1 and CDK7, exhibiting IC50 values of 893 nM and 248 nM, respectively. This compound effectively inhibits the proliferation of cancer cell lines, including MDA-MB-231, MCF-7, A549, and HCT-116. Additionally, HDAC1/CDK7-IN-1 induces cell cycle arrest and apoptosis specifically in HCT-116 cells, while also disrupting their migratory capacity. These properties make it a valuable tool for cancer research, particularly in exploring therapeutic strategies that target epigenetic regulation and cell cycle dynamics. -
PLK1 Inhibtor
PLK1-IN-13 is a selective inhibitor of polo-like kinase 1 (PLK1) with an IC50 of 0.27 nM, exhibiting oral bioavailability. It also demonstrates inhibitory activity against PLK2 and PLK3, with IC50 values of 12.72 nM and 4.12 nM, respectively. PLK1-IN-13 effectively induces G2 phase cell cycle arrest, promotes apoptosis, and down-regulates the c-MYC oncogene, which is associated with tumor proliferation. This compound is particularly relevant for research on acute myeloid leukemia (AML) and other cancer models. -
PLK1 Inhibitor
PLK1-IN-15 is a potent inhibitor of Polo-like Kinase 1 (PLK1) with an IC50 of 38.5 nM. It demonstrates significant antiproliferative effects in various cancer cell lines, including HepG2, Huh7, H1299, and A549, with IC50 values of 2.03, 2.08, 4.79, and 17.11 μM, respectively. PLK1-IN-15 is known to induce cell cycle arrest at the G2/M phase and trigger apoptosis, underscoring its potential as an effective agent in cancer research and therapeutic development. -
CDK Inhibitor
5,6-Dichlorobenzimidazole riboside (DRB) functions as a selective inhibitor of several carboxyl-terminal domain kinases, notably casein kinase II and cell cycle-dependent kinases (CDKs). This nucleoside analog exhibits antitumor activity and has been shown to induce apoptosis in targeted cancer cells. Its role in modulating kinase activity makes DRB valuable for research in cancer biology and cell cycle regulation. -
CDK9 Inhibitor
Enitociclib is a highly selective CDK9 inhibitor, with an IC50 value of 3 nM, that disrupts transcriptional elongation by inhibiting Ser2/Ser5 phosphorylation of RNA polymerase II. This compound specifically targets and depletes short-lived oncogenic proteins such as c-MYC and MCL-1, thereby inducing apoptosis in tumor cells. Enitociclib also impairs enhancer RNA production and enhancer-promoter interactions, leading to downregulation of oncogene expression at the epigenetic level. Its efficacy is demonstrated through synergistic interactions with agents like Bortezomib, Lenalidomide, Pomalidomide, Venetoclax, and Paclitaxel, providing a valuable research tool for studying malignancies such as double-hit diffuse large B-cell lymphoma, multiple myeloma, and pancreatic ductal adenocarcinoma. -
PLK2 Inhibitor
ON1231320 is a selective inhibitor of polo-like kinase 2 (PLK2), exhibiting an IC50 of 0.31 μM. This compound disrupts tumor cell cycle progression specifically at the G2/M phase during mitosis, leading to apoptotic cell death. The arylsulfonyl pyrido-pyrimidinone structure contributes to its significant antitumor activity, making ON1231320 a valuable tool for research in cancer biology and therapeutic development. -
BRCA2-RAD51 Interaction Inhibitor
CAM833 is a potent orthosteric inhibitor of the BRCA2-RAD51 interaction, exhibiting a Kd of 366 nM against ChimRAD51 protein. This compound also disrupts RAD51 oligomerization, leading to enhanced progression of G2/M-arrested cells into apoptosis. CAM833 is valuable for research applications aimed at studying DNA repair mechanisms and therapeutic strategies in BRCA2-related cancers. -
CDK Inhibitor
Borrelidin is a CDK inhibitor that acts by targeting threonyl-tRNA synthetase, isolating from the bacterium Streptomyces rochei. This compound demonstrates potent angiogenesis inhibition with an IC50 of 0.8 nM and induces apoptosis in endothelial tube-forming cells. Additionally, Borrelidin possesses significant antimalarial activity, exhibiting IC50 values of 1.9 nM and 1.8 nM against the K1 and FCR3 strains of Plasmodium falciparum, respectively. These properties make Borrelidin a valuable tool for research in cancer and malaria biology. -
CDK9 Inhibitor
NSC 107512 is a potent inhibitor of cyclin-dependent kinase 9 (CDK9). As a member of the sangivamycin-like molecule class, it demonstrates significant biological activity by inhibiting cellular growth and inducing apoptosis in multiple myeloma tumors. This compound is valuable for research applications focused on cancer biology and the exploration of therapeutic strategies targeting CDK9-mediated pathways. -
CDK9 Inhibitor
AZ5576 is a potent and highly selective inhibitor of cyclin-dependent kinase 9 (CDK9), with an IC50 value of less than 5 nM. This compound effectively inhibits the phosphorylation of RNA polymerase II at Ser2, leading to a reduction in transcriptional elongation. AZ5576 is applicable in the research of hematological malignancies, aiding in the understanding of transcription regulation in cancer biology. -
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.
