Catalog No.
Product Name
Application
Product Information
Citations
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PLK1/BRD4 Inhibitor
PLK1/BRD4-IN-5 is a potent inhibitor targeting both PLK1 and BRD4, exhibiting IC50 values of 0.3 nM and 60.8 nM, respectively. This compound effectively induces cell cycle arrest in the S phase and promotes apoptosis in MV4-11 cells in a dose-dependent manner. PLK1/BRD4-IN-5 is a valuable tool for cancer research, facilitating studies on mechanisms of tumorigenesis and therapeutic responses. -
CDK8 Inhibitor
CDK8-IN-13 is a potent and selective inhibitor of cyclin-dependent kinase 8 (CDK8), exhibiting an IC50 value of 51.9 nM. This compound induces apoptosis and modulates the expression of phosphorylated STAT1 at serine 727 and STAT5 at serine 726. Due to its antitumor properties, CDK8-IN-13 is valuable for research applications focusing on cancer biology and therapeutic development targeting the CDK8 pathway. -
c-Myc Inhibitor
CMLD010509 is a selective inhibitor of c-Myc, targeting the oncogenic translation program associated with multiple myeloma (MM). This compound demonstrates an IC50 of less than 10 nM in various MM cell lines and effectively induces apoptosis. CMLD010509 operates through a phosphorylation-independent mechanism, making it a valuable tool for studying the role of translation in oncogenesis and developing targeted therapeutic strategies in MM research. -
CCND1/CDK4 PROTAC Degrader
CPD-10 is a targeted CCND1 and CDK4 PROTAC degrader that effectively promotes the degradation of these proteins. Exhibiting significant anti-proliferative activity, CPD-10 induces apoptosis in cancer cell lines. It decreases the expression levels of cyclin D1, cyclin D3, CDK4, and phosphorylated Rb at serines 5807 and 811 in a dose-dependent manner, making it a valuable tool for research in cancer biology and therapeutic applications targeting cell cycle regulation. -
CDK7 Inhibitor
Samuraciclib is a selective, ATP-competitive inhibitor of CDK7, exhibiting an IC50 of 41 nM. This compound demonstrates significant selectivity over CDK1, CDK2, CDK5, and CDK9, with fold selectivities of 45, 15, 230, and 30, respectively. Samuraciclib effectively inhibits the proliferation of breast cancer cell lines, with GI50 values ranging from 0.2 to 0.3 μM, indicating its potential as an effective therapeutic agent in oncology research. -
CDK1 Inhibitor
Avotaciclib trihydrochloride is an orally active inhibitor of cyclin-dependent kinase 1 (CDK1). This compound has demonstrated the ability to inhibit tumor cell proliferation and induce apoptosis, making it a valuable tool for cancer research. Avotaciclib trihydrochloride is particularly relevant for studies focused on pancreatic and lung cancers. -
CDK4 Inhibitor
CDK4-IN-3 is a potent irreversible inhibitor of cyclin-dependent kinase 4 (CDK4), exhibiting an IC50 of 25 nM and demonstrating over 10-fold selectivity for CDK4 compared to CDK6. This compound effectively arrests the cell cycle in the G₁ phase, leading to the induction of apoptosis in tumor cells. CDK4-IN-3 is valuable for research applications focused on solid tumors, including breast and lung cancers. -
CDK1 Inhibitor
CGP-74514 is a potent and selective inhibitor of cyclin-dependent kinase 1 (CDK1), exhibiting an IC50 of 25 nM. By targeting the CDK1/cyclin B complex, CGP-74514 effectively halts the cell cycle at the G2/M phase and triggers apoptosis in tumor cells. This compound is particularly valuable for research focused on bladder cancer and related therapeutic applications. -
PROTAC CDK4/6 degrader
HEMTAC CDK4/6 degrader 1 is a PROTAC designed to target CDK4 and CDK6 through a dual-ligand approach involving HSP90. This compound effectively induces the degradation of CDK4/6 in B16F10 melanoma cells, leading to cell cycle arrest at the G0/G1 phase and subsequent apoptosis. It serves as a vital tool for cancer research, particularly in elucidating mechanisms of CDK4/6 regulation and their role in tumor progression. Additionally, HEMTAC CDK4/6 degrader 1 features an alkyne functional group, enabling copper-catalyzed azide-alkyne cycloaddition (CuAAc) with azide-containing compounds for advanced applications in chemical biology. -
G-quadruplexes Stabilizer
L5-DA is a selective G-quadruplex stabilizer that preferentially interacts with G4 structures over double-stranded DNA. This compound exhibits notable cytotoxicity against HeLa cells, with an IC50 value of 4.3 μM. L5-DA effectively stabilizes G4s within HeLa cells, leading to the induction of apoptosis and cell cycle arrest. Its role in modulating G-quadruplexes makes it a valuable tool for research in cancer biology and therapeutic development. -
CDK Inhibitor
CDK9-IN-7 is a selective and potent inhibitor of cyclin-dependent kinase 9 (CDK9), demonstrating an IC50 of 11 nM. This compound selectively inhibits CDK9 over other cyclin-dependent kinases, such as CDK4 and CDK6, with IC50 values of 148 nM and 145 nM, respectively. CDK9-IN-7 exhibits significant antitumor activity, inducing apoptosis in non-small cell lung cancer (NSCLC) cells, arresting the cell cycle in the G2 phase, and reducing the stemness characteristics of NSCLC. It is a valuable tool for research into cancer biology and potential therapeutic applications. -
G-quadruplex Stabilizer
MTR-106 is a potent G-quadruplex stabilizer that also functions as an RNA polymerase I inhibitor. This compound has demonstrated the ability to induce apoptosis and inhibit cell proliferation, making it a valuable tool in cancer research. Its unique mechanism of action provides insights into G-quadruplex dynamics and their implications in tumor biology. -
CHKα Inhibitor
ICL-CCIC-0019 is a potent inhibitor of choline kinase α (CHKα), a key enzyme involved in phosphatidylcholine synthesis and cellular signaling. This compound has been shown to induce a G1 phase cell cycle arrest and promote endoplasmic reticulum stress-mediated apoptosis in various cancer cell lines. ICL-CCIC-0019 is valuable for research applications focused on cancer biology, specifically in studies exploring cell cycle regulation and mechanisms of apoptosis in tumor cells. -
ROCK Inhibitor
RKI-1447 dihydrochloride is a selective inhibitor of Rho-associated kinase (ROCK), exhibiting IC50 values of 14.5 nM and 6.2 nM for ROCK1 and ROCK2, respectively. This compound effectively suppresses the growth of colorectal carcinoma cells while inducing apoptosis, making it a valuable tool for research in cancer biology and therapeutics targeting ROCK signaling pathways. -
KRAS G12D Inhibitor
KRAS G12D inhibitor 14 is a selective inhibitor targeting the KRAS G12D mutation, exhibiting a binding affinity (KD) of 33 nM. This compound effectively reduces the levels of active KRAS G12D (KRAS G12D-GTP) without impacting the KRAS G13D variant. It is a valuable tool for research applications focused on elucidating the role of KRAS G12D in oncogenic signaling pathways and developing targeted cancer therapies. -
Pan-CDK Inhibitor
AG-012986 is a potent pan-CDK inhibitor targeting multiple cyclin-dependent kinases including CDK1, CDK2, CDK4, CDK5, CDK6, and CDK9. It demonstrates significant biological activity with Kis of 9.2 nM for CDK4/cyclin, 44 nM for CDK1/cyclin B, and 94 nM for CDK2/cyclin A, alongside IC50 values of 4 nM for CDK9/cyclin T and 22 nM for CDK5/p35. AG-012986 effectively inhibits cell proliferation in cancer cell lines, inducing cell cycle arrest and apoptosis, making it a valuable tool for cancer research and therapeutic development. -
CDK2/JAK2/FLT3 Inhibitor
(E/Z)-Zotiraciclib hydrochloride is a potent inhibitor of CDK2, JAK2, and FLT3, exhibiting IC50 values of 13 nM, 73 nM, and 56 nM, respectively. This orally active compound demonstrates significant efficacy in inhibiting the proliferation of various cancer cell lines. It is a valuable tool for research into therapeutic strategies targeting cell cycle regulation and signal transduction pathways in cancer. -
CDK Inhibitor
RGB-286638 free base is a potent CDK inhibitor targeting cyclin T1-CDK9, cyclin B1-CDK1, cyclin E-CDK2, cyclin D1-CDK4, cyclin E-CDK3, and p35-CDK5, with IC50 values of 1, 2, 3, 4, 5, and 5 nM, respectively. Additionally, it inhibits GSK-3β, TAK1, Jak2, and MEK1, exhibiting IC50 values of 3, 5, 50, and 54 nM. This compound is valuable for research in cell cycle regulation, cancer therapeutics, and signaling pathways involving kinase activity. -
CDK2/JAK2/FLT3 Inhibitor
(E/Z)-Zotiraciclib citrate is a potent inhibitor targeting CDK2, JAK2, and FLT3 kinases. This compound demonstrates significant biological activity in disrupting cell cycle progression and signaling pathways associated with cell proliferation and survival. It is utilized in cancer research applications, particularly for studies involving hematological malignancies and solid tumors where these kinases are dysregulated. -
CDK2/JAK2/FLT3 Inhibitor
Zotiraciclib hydrochloride is a novel small molecule inhibitor targeting cyclin-dependent kinase 2 (CDK2), Janus kinase 2 (JAK2), and Fms-like tyrosine kinase 3 (FLT3). This reagent demonstrates anti-tumor activity by downregulating the Myc oncogene through CDK9 inhibition, contributing to reduced tumor growth. Zotiraciclib hydrochloride is particularly relevant for research into cancers capable of crossing the blood-brain barrier, and elevated levels of the MCL-1 protein may indicate its potential as a prognostic marker and therapeutic target in cancer studies. -
Aurora Kinase A/JAK2 Inhibitor
AJI-100 is a dual-target inhibitor that selectively inhibits Aurora kinase A and JAK2 with IC50 values of 12.7 nM and 18.5 nM, respectively. By directly blocking Aurora kinase A, AJI-100 disrupts T cell mitosis and cell polarity, while its inhibitory effect on JAK2 activation prevents STAT3 phosphorylation. This compound is valuable for research focused on modulating immune responses and has potential applications in the prevention of graft-versus-host disease (GVHD). -
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. -
CDK9/FLT3 Inhibitor
CDDD11-8 is a potent and selective inhibitor of cyclin-dependent kinase 9 (CDK9) and FLT3-ITD, exhibiting Ki values of 8 nM and 13 nM, respectively. This compound effectively reduces the proliferation of leukemia cell lines, particularly those associated with the FLT3-ITD mutation. CDDD11-8 serves as a valuable tool for research into targeted therapies for hematological malignancies, specifically in the study of cell cycle regulation and tyrosine kinase signaling pathways. -
Dual FLT3/CHK1 Inhibitor
FLT3/CHK1-IN-1 is a dual inhibitor targeting both FLT3 and CHK1, demonstrating significant selectivity for c-KIT over other kinases. With an IC50 value of 58.4 μM, it shows reduced affinity for the hERG channel, minimizing potential cardiac side effects. FLT3/CHK1-IN-1 has exhibited efficacy in inhibiting tumor growth in mouse xenotransplantation models with MV-4-11 cells, making it a valuable tool for cancer research and therapeutic development. -
FLT3/CDK5 Inhibitor
AMG 925 (HCl) is a potent dual inhibitor targeting FLT3 and CDK5, demonstrating IC50 values of 2±1 nM and 3±1 nM, respectively. This compound exhibits selectivity for these kinases, making it a valuable tool for research into hematological malignancies and cancer progression. Its oral bioavailability further enhances its utility in preclinical studies investigating therapeutic interventions for FLT3-driven malignancies and CDK5-associated diseases. -
FLT3/CDK4 Inhibitor
FLT3/CDK4-IN-1 is a highly selective, orally active dual inhibitor targeting FLT3 and CDK4, demonstrating IC50 values of 11 nM and 7 nM, respectively. This compound exhibits significant antiproliferative activity against specific cancer cell lines and shows promising antitumor effects in vivo. FLT3/CDK4-IN-1 is suitable for research applications focused on cancer biology, particularly in exploring pathways associated with leukemias and solid tumors. -
PLK4 Inhibitor
CZS-241 is a selective Polo-like Kinase 4 (PLK4) inhibitor, exhibiting an IC50 of 2.6 nM. In addition to its primary activity, CZS-241 also inhibits TRKA with an IC50 of 2.74 μM. This compound induces apoptosis and effectively arrests the cell cycle at the S/G2 phase. CZS-241 demonstrates potent antiproliferative effects against leukemia cell lines while maintaining safety profiles in normal cell lines, making it a valuable tool for cancer research. -
CDK Inhibitor
(E/Z)-SU9516 is a selective inhibitor of cyclin-dependent kinases (CDKs), primarily targeting CDK2, with an IC50 value of 22 nM. This compound also exhibits inhibitory effects on CDK1 and CDK4, with IC50 values of 40 nM and 200 nM, respectively. Its potent inhibition of CDKs makes (E/Z)-SU9516 a valuable tool for studying cell cycle regulation and therapeutic applications in cancer research. -
c-Myc Inhibitor
Y502-3888 is a selective c-Myc inhibitor that targets the G-quadruplex (G4) structure of c-Myc, effectively impairing its transcriptional activity. This compound downregulates c-Myc expression at both mRNA and protein levels, leading to reduced viability and induced apoptosis in myeloma cells. Y502-3888 serves as a valuable tool for investigating the role of c-Myc in multiple myeloma and other related malignancies. -
CDK4 Inhibitor
3-ATA is a selective inhibitor of cyclin-dependent kinase 4 (CDK4), demonstrating both neuroprotective and antitumor properties. This compound has been shown to reduce kainic acid-induced apoptosis in cerebellar granule neurons, making it a valuable tool for investigating neurodegenerative diseases. Its ability to modulate cell cycle progression and prevent neuronal death highlights its potential applications in both cancer research and neuroprotection studies. -
CDK9-Cyclin T1 PPI Inhibitor
CDK9-Cyclin T1 PPI-IN-1 is a selective inhibitor of the CDK9-Cyclin T1 protein-protein interaction. This compound effectively inhibits cell proliferation in triple-negative breast cancer (TNBC) MDA-MB-231 cells with an IC50 of 0.044 μM and promotes apoptosis. Additionally, CDK9-Cyclin T1 PPI-IN-1 suppresses CDK9 transcriptional activity and diminishes the phosphorylation of RNA Polymerase II at the CTD serine 2 residue. In vivo studies further demonstrate its capability to inhibit tumor growth in a TNBC 4T1 mouse model. -
CDK Inhibitor
CDK-IN-9 is a potent cyclin-dependent kinase (CDK) inhibitor that serves as a molecular glue, promoting the interaction between CDK12 and DDB1. With an IC50 value of 4 nM for CDK2/E, CDK-IN-9 facilitates the polyubiquitination and subsequent degradation of cyclin K. Additionally, it induces apoptosis through the dephosphorylation of retinoblastoma protein and RNA polymerase II, making it a valuable tool for research in cancer biology and cell cycle regulation. -
PROTAC CDK4/6/9 Degrader
PROTAC CDK4/6/9 Degrader 1 is a targeted protein degradation agent that specifically degrades cyclin-dependent kinases CDK4, CDK6, and CDK9. This compound effectively inhibits the proliferation of triple-negative breast cancer (TNBC) cells by inducing G1 phase arrest, promoting apoptosis, and suppressing cellular migration and invasion. PROTAC CDK4/6/9 Degrader 1 serves as a valuable tool for studying the role of these kinases in TNBC and may support the development of novel therapeutic strategies aimed at this aggressive cancer subtype. -
c-Myc G4 Stabilizer
GQC-05 is a selective c-Myc G-quadruplex (c-Myc G4) stabilizer that demonstrates potent activity with KD values ranging from 0.1 to 1.43 μM. This compound effectively reduces c-Myc expression, leading to the induction of apoptosis in cancer cells. GQC-05 serves as a valuable tool in cancer research, particularly in studying conditions such as Burkitt lymphoma. -
CDK4/CDK6 Inhibitor
CDK4/6-IN-10 is a potent and selective inhibitor of CDK4 and CDK6, exhibiting IC50 values of 22 nM and 10 nM, respectively. This compound demonstrates significant antitumor activity and is particularly relevant for research targeting multiple myeloma (MM). Its oral bioavailability combined with its selectivity makes CDK4/6-IN-10 a valuable tool for investigating the therapeutic potential in cancer biology. -
PARP1/2/CDK12 Inhibitor
PARP-1/2-IN-2 is a potent inhibitor of PARP1, PARP2, and CDK12, exhibiting IC50 values of 34 nM, 30 nM, and 285 nM, respectively. This compound disrupts DNA damage repair mechanisms, leading to induced cell cycle arrest and apoptosis. Notable for its efficacy in targeted therapy, PARP-1/2-IN-2 effectively inhibits the growth of triple-negative breast cancer (TNBC) cells and demonstrates significant antitumor activity in TNBC xenograft models. This makes it a valuable tool for research in cancer biology and therapeutic development. -
Aurora-A kinase Inhibitor
LY3295668 erbumine is a potent and selective inhibitor of Aurora-A kinase, exhibiting a Ki value of 0.8 nM for AurA while demonstrating significantly lower binding affinity for AurB at 1038 nM. This compound effectively inhibits the autophosphorylation of Aurora-A, leading to mitotic arrest and apoptosis without promoting polyploidy associated with AurB inhibition. LY3295668 erbumine is valuable for research into small cell lung cancer and other conditions involving dysregulation of Aurora kinases. -
CDK1 Inhibitor
Avotaciclib sulfate is an orally bioavailable inhibitor of cyclin-dependent kinase 1 (CDK1). It effectively inhibits cell proliferation and induces apoptosis in various cancer cell lines. This compound is particularly useful for research applications focused on oncology, including the study of pancreatic and lung cancer. -
c-Myc G4 Inhibitor
c-Myc inhibitor 16 iodide is a selective inhibitor of the c-Myc G-quadruplex, effectively targeting the c-Myc gene's transcription and translation processes. It disrupts the tumor cell cycle by arresting growth in the G0/G1 phase and activates the mitochondrial apoptosis pathway, leading to early apoptosis in cancer cells. This compound has significant potential in research applications related to breast cancer. -
Aurora B Inhibitor
HOI-07 is a selective inhibitor of Aurora B kinase that interferes with the phosphorylation of histone H3 at Ser10 in lung cancer cells. This compound induces cell-cycle arrest and apoptosis, demonstrating significant antitumor activity. HOI-07 effectively suppresses tumor growth in xenograft models, including A549, 143B, and KHOS, making it a valuable tool for cancer research and therapeutic investigation. -
c-Myc Inhibitor
EP12 is a selective c-Myc inhibitor that stabilizes c-Myc G-quadruplexes. This compound induces apoptosis and causes DNA damage in multiple myeloma cells, effectively inhibiting their growth. Additionally, EP12 disrupts the nuclear translocation of P65/P50 by interfering with the NF-κB signaling pathway, highlighting its potential in cancer research and therapeutic applications. -
PKMYT1 Inhibitor
XH-30 is a potent and selective inhibitor of PKMYT1, exhibiting an IC50 of 4.1 nM. This compound effectively suppresses the proliferation of P53-mutated triple-negative breast cancer (TNBC) cells by promoting G2/M phase release, inducing DNA damage, and triggering apoptosis. Additionally, XH-30 demonstrates significant antitumor effects in MDA-MB-231 mouse models, making it a valuable tool for research focused on P53-mutated TNBC. -
CHK1 Inhibitor
CHK1-IN-12 is a potent and selective checkpoint kinase 1 (CHK1) inhibitor that exerts its effects by significantly reducing CHK1 phosphorylation activity, thereby disrupting the DNA damage response pathway. With an in vitro enzyme IC50 of up to 10 nM and a cellular IC50 of 50 nM, CHK1-IN-12 effectively induces cell cycle arrest and apoptosis in tumor cells. This compound holds potential for cancer research, particularly in studies focused on cell cycle regulation and DNA repair mechanisms. -
CDK12/CDK13 Inhibitor
ZSQ836 is an orally active dual covalent inhibitor of CDK12 and CDK13, demonstrating an EC50 value of 32 nM for CDK12 inhibition. This compound has been shown to induce apoptosis and exhibits significant anticancer efficacy in vivo. ZSQ836 is a valuable tool for investigating the mechanisms and treatment strategies associated with ovarian cancer. -
PLK1 Inhibitor
PLK1-IN-16 is a potent and selective inhibitor of polo-like kinase 1 (PLK1) with an IC50 value of 0.25 nM. This compound is primarily utilized in cancer research due to its ability to induce G2 phase cell cycle arrest and promote apoptosis, displaying significant antiproliferative activity against various tumor cell lines. Additionally, PLK1-IN-16 has been shown to exhibit stability under simulated gastric acid conditions and presents manageable CYP 450 inhibition. Its applications extend to the study of triple-negative breast cancer (TNBC), breast cancer, and leukemia. -
PLK4 Inhibitor
Ocifisertib hydrochloride is a potent inhibitor of Polo-like kinase 4 (PLK4) with a Ki value of 0.26 nM and an IC50 of 2.8 nM. This compound demonstrates significant biological activity by inhibiting the growth of various cancer cell lines, inducing cell cycle arrest at the G2/M phase, and promoting apoptosis. Research applications include evaluating its antitumor efficacy in preclinical models, making it a valuable reagent for studying mechanisms of cancer progression and potential therapeutic strategies. -
CHK1 Inhibitor
Prexasertib lactate is a selective ATP-competitive inhibitor of checkpoint kinase 1 (CHK1), with a Ki value 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 leading to replication catastrophe, Prexasertib lactate promotes apoptosis in cancer cells. Its potent anti-tumor efficacy makes it a valuable tool for cancer research and therapeutic development. -
Telomeric G-Quadruplex Ligand
Telomeric G4s ligand 1 is a telomeric G-quadruplex ligand known for its ability to stabilize telomeric G4 structures and promote R-loop formation, resulting in DNA damage responses. This compound has been shown to induce apoptosis in tumor cells and trigger immunogenic cell death (ICD), making it a valuable tool for cancer research and therapeutic applications. -
c-Myc Inhibitor
(-)-CMLD010509 is a potent c-Myc inhibitor that selectively targets the oncogenic translation program associated with multiple myeloma. This compound demonstrates significant activity, exhibiting an IC50 of less than 10 nM in various multiple myeloma cell lines, leading to the induction of apoptosis. (-)-CMLD010509 operates through a mechanism that is independent of eIF4E phosphorylation, making it a valuable tool for studying the translation control of key oncoproteins such as MYC, MDM2, CCND1, MAF, and MCL-1. -
CDK Inhibitor
R547 mesylate is a potent and selective ATP-competitive inhibitor of cyclin-dependent kinases (CDKs). It exhibits inhibitory constants of 2 nM for CDK1/cyclin B, 3 nM for CDK2/cyclin E, and 1 nM for CDK4/cyclin D1. Due to its oral bioavailability and high specificity, R547 mesylate is valuable for investigating cell cycle regulation and the role of CDKs in cancer research.
