Catalog No.
Product Name
Application
Product Information
Citations
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Tyrosinase Inhibitor
Norartocarpetin is a potent tyrosinase inhibitor, demonstrating significant inhibition with an IC50 value of 0.47 μM. This compound serves as an effective antibrowning agent for food systems research and exhibits notable anticancer activity against lung carcinoma cells (NCI-H460) with an IC50 of 22 μM. Its antiproliferative effects are mediated through targeting the Ras/Raf/MAPK signaling pathway, inducing mitochondrial-mediated apoptosis, causing S-phase cell cycle arrest, and inhibiting cell migration and invasion in human lung carcinoma cells. -
Ras-related GTPases Activator
ML-097 is a potent activator of Ras-related GTPases, specifically targeting Rac1, CDC42, Ras, and Rab7. It plays a critical role in modulating cellular signaling pathways associated with proliferation, migration, and cytoskeletal organization. This compound is valuable for research applications focusing on cancer biology, neurobiology, and cellular communication mechanisms. -
RAS-Effector PPI Inhibitor
RAS inhibitor Abd-7 is a selective RAS-binding compound (Kd=51 nM) that disrupts RAS-effector protein-protein interactions. This inhibitor effectively interferes with RAS-dependent signaling pathways by preventing the interactions between RAS and key effectors such as PI3K, CRAF, and RALGDS, as well as mutant KRAS proteins, NRAS Q61H, and HRAS G12V. RAS inhibitor Abd-7 is valuable for research applications targeting RAS-mediated processes in cancer biology. -
KRAS(G12C) Inhibitor
BBO-8520 is a selective covalent inhibitor of the KRAS G12C mutation, effectively promoting the inactive (OFF) state of KRAS by blocking GTP binding. This compound inhibits cell proliferation and disrupts the interaction between RAS and RAF1, leading to significant impact on oncogenic signaling pathways. BBO-8520 is suitable for research applications focusing on cancer biology and therapeutic strategies targeting KRAS-driven tumors. -
Rab27a-JFC1 Inhibitor
Nexinhib20 is a selective inhibitor of the Rab27a-JFC1 interaction (IC50: 2.6 μM) and Rac-1-GTP signaling. This compound effectively inhibits neutrophil exocytosis, adhesion, and β2 integrin activation, demonstrating significant anti-inflammatory properties. Nexinhib20 is suitable for research applications focused on systemic inflammation and myocardial ischemia-reperfusion injury. -
Epac Activator
8-pCPT-2′-O-Me-cAMP sodium is an analog of cyclic AMP that serves as a selective activator of exchange proteins activated by cAMP (Epac). This compound demonstrates effective activation of Epac1 with an EC50 value of 2.2 μM, while showing minimal activity towards protein kinase A (EC50 >10 μM). In vitro studies highlight its role in stimulating Epac-mediated Ca2+ release in pancreatic β-cells, and it functions as an activator of Rap1. Additionally, 8-pCPT-2′-O-Me-cAMP sodium has been shown to strengthen the barrier of retinal pigment epithelium against pathological choroidal endothelial cell invasion, contributing to research on macular degeneration. -
KRas Inhibitor
Pan KRas-IN-1 is a pan KRas inhibitor that targets mutant KRas proteins, particularly effective against KRas G12C inhibitor-resistant cancer models. It exhibits potent anti-cancer activity by disrupting KRas signaling pathways, thereby inhibiting tumor cell proliferation and survival. This compound is valuable in research applications focused on overcoming resistance mechanisms in KRas-driven malignancies. -
PROTAC Degrader
SNX7886 is a potent PROTAC degrader targeting CDK8 and CDK19. It effectively induces degradation of CDK8 and CDK19, achieving up to 90% and 80% degradation, respectively, in 293 cells. This compound is valuable for research applications in understanding the role of CDK8/19 in various biological processes and cancer pathways. -
PROTAC KRAS G12C Degrader
PROTAC KRAS G12C degrader-1 is a Cereblon-based PROTAC targeting the KRAS G12C mutant. This compound promotes the formation of a dimer between Cereblon and KRAS G12C, leading to the degradation of GFP-tagged KRAS G12C in reporter cell systems. It serves as a valuable tool for research on targeted degradation strategies in KRAS-driven cancers. -
Kinases PROTAC
DB1113 is a bifunctional compound designed for targeted protein degradation of various kinases. It effectively induces degradation of ABL1, ABL2, BLK, CDK4, CDK11B, EPHA3, MAPK7, RIPK1, and others, facilitating the investigation of kinase-related signaling pathways. DB1113 is suitable for research focusing on diseases or disorders associated with dysregulated kinase activity, providing a valuable tool for exploring therapeutic interventions in cancer and other conditions. -
PROTAC CDK4/6 Degrader
BSJ-02-162 is a potent PROTAC degrader targeting CDK4/6 through the utilization of a thalidomide-based E3 ligase ligand and a selective CDK4/6 inhibitor. This compound effectively recruits ubiquitin ligases to facilitate the targeted degradation of CDK4/6, thereby modulating cellular responses to cell cycle regulation. BSJ-02-162 is designed for research applications exploring cancer therapies and the mechanisms of protein homeostasis within tumor cells. -
CDK2 molecular glue Degrader
CDK2 degrader 1 is a selective molecular glue degrader targeting cyclin-dependent kinase 2 (CDK2). It effectively induces ubiquitination and proteasomal degradation of CDK2 by binding to cereblon, achieving a Dmax greater than 80% and a Ki greater than 1 μM. This compound is utilized in cancer research, providing insights into tumor biology and potential therapeutic strategies. -
CDK Inhibitor
(S)-CR8 is a selective inhibitor of cyclin-dependent kinases (CDKs), demonstrating potent inhibitory activity with IC50 values of 0.060 μM for CDK2/cyclin E, 0.080 μM for CDK2/cyclin A, 0.11 μM for CDK9/cyclin T, 0.12 μM for CDK5/p25, and 0.15 μM for CDK1/cyclin B. This compound effectively reduces the survival of SH-SY5Y cells, with an IC50 of 0.40 μM, making it a valuable tool for studying cell cycle regulation and potential therapeutic strategies in cancer research. -
CDK Inhibitor
Aloisine A is a potent cyclin-dependent kinase (CDK) inhibitor, exhibiting IC50 values of 0.15 μM for CDK1/cyclin B, 0.12 μM for CDK2/cyclin A, 0.4 μM for CDK2/cyclin E, and 0.16 μM for CDK5/p35. In addition to its CDK inhibitory effects, Aloisine A also inhibits GSK-3α and GSK-3β with IC50 values of 0.5 μM and 1.5 μM, respectively. Notably, it enhances the activity of wild-type and mutant CFTR with submicromolar affinity through a cAMP-independent mechanism, making it a valuable tool for research related to cystic fibrosis and CFTR-related disorders. -
CDK Inhibitor
NSC693868 is a selective inhibitor of cyclin-dependent kinases CDK1 and CDK5, demonstrating IC50 values of 600 nM and 400 nM, respectively. This compound also exhibits weaker inhibition of GSK3β with an IC50 of 1 µM and does not affect CDC25 activity. NSC693868 is employed in research to elucidate the functions of CDK1 and CDK5 within various cellular signaling pathways. -
GSK-3α/β Inhibitor
(E/Z)-BIO-acetoxime is a potent and selective inhibitor of GSK-3α/β, exhibiting an IC50 of 10 nM. This compound demonstrates exceptional selectivity with over 200-fold preference against CDK5/p25, CDK2/cyclin A, and CDK1/cyclin B, with IC50 values of 2.4, 4.3, and 63 μM, respectively. Its strong inhibitory activity makes it a valuable tool for research focused on signaling pathways involved in cell proliferation, differentiation, and apoptosis. -
Cdc42 GTPase Inhibitor
ML141 (CID-2950007) is a potent, allosteric, selective and reversible non-competitive inhibitor of Cdc42 GTPase. ML141 inhibits Cdc42 wild type and Cdc42 Q61L mutant with EC50s of 2.1 and 2.6 μM, respectively. ML141 shows low micromolar potency and selectivity against other members of the Rho family of GTPases (Rac1, Rab2, Rab7). ML141 do not show cytotoxicity in multiple cell lines. -
CDK9 Inhibitor
Tambiciclib is a potent and selective CDK9 inhibitor with an IC50 of 1 nM, exhibiting over 200-fold selectivity against other cyclin-dependent kinases and significant selectivity over DYRK1A/B and a wide range of kinases. This compound has demonstrated effective in vitro and in vivo antileukemic activity in acute myeloid leukemia (AML) models by inhibiting RNA Polymerase II phosphorylation, leading to downregulation of MCL1 and MYC, and subsequent induction of apoptosis. Tambiciclib is suitable for research applications focused on AML and related oncological studies. -
Cyclin/CDK Inhibitor
VMY-1-103 is a selective inhibitor of the cyclin-dependent kinase (CDK) complex, effectively arresting the cell cycle at the G1 phase. It has been demonstrated to reduce mitochondrial membrane potential, induce p53 phosphorylation, and trigger PARP cleavage, ultimately activating caspase-3 and initiating apoptosis in LNCaP prostate cancer cells. This compound is valuable for research applications focused on cancer biology and the mechanisms of cell cycle regulation and apoptosis. -
CDK2/4/6 PROTAC Degrader
PROTAC CDK2/4/6 Degrader-2 is a targeted protein degradator specifically designed to degrade cyclin-dependent kinases CDK2, CDK4, and CDK6. This compound effectively inhibits cell proliferation and induces cell cycle arrest and apoptosis in malignant melanoma cells. Its application extends to cancer research, particularly in investigating the role of CDK2/4/6 in tumor biology. The compound can also be converted into its prodrug form, enabling versatile utilization in various assays related to cancer therapeutics. -
KDM1/CDK1 Inhibitor
KDM1/CDK1-IN-1 is a potent inhibitor of both KDM1 and CDK1, exhibiting IC50 values of 0.096 μM and 0.078 μM, respectively. This compound effectively induces cell cycle arrest at the G2/M phase and promotes apoptosis in HOP-92 cancer cells. Additionally, KDM1/CDK1-IN-1 demonstrates significant cytotoxic effects against a range of cell lines, including CCRF-CEM, HOP-92, and Hep-G2, with IC50 values of 16.34 μM, 3.45 μM, and 7.79 μM, respectively. Its ability to target critical regulators of the cell cycle makes KDM1/CDK1-IN-1 valuable for cancer research applications. -
CDK1 Inhibitor
Avotaciclib is an orally active inhibitor of cyclin-dependent kinase 1 (CDK1). It effectively inhibits tumor cell proliferation and induces apoptosis, making it a valuable compound for cancer research. This reagent is particularly relevant in the study of cancers, including pancreatic and lung cancer, where CDK1 plays a critical role in cell cycle regulation and tumor growth. -
DYRKs/CLKs Inhibitor
Leucettine L41 is a potent inhibitor of dual-specificity tyrosine phosphorylation-regulated kinases (DYRKs) and CDC-like kinases (CLKs). This compound also modulates GSK-3 signaling, demonstrating significant effects on cellular processes by inhibiting apoptosis and reducing reactive oxygen species (ROS) production. Leucettine L41 promotes cell cycle progression and proliferation in β-cells, enhancing insulin secretion. It is a valuable tool for research focused on neurological disorders, including Alzheimer’s disease, and metabolic diseases such as diabetes. -
CHK1 Inhibitor
Prexasertib dimesylate is a selective checkpoint kinase 1 (CHK1) inhibitor that functions as an ATP-competitive agent. With a Ki of 0.9 nM and an IC50 of less than 1 nM, it effectively inhibits CHK2 and RSK1, exhibiting IC50 values of 8 nM and 9 nM, respectively. This compound induces double-stranded DNA breaks and replication catastrophe, leading to apoptosis. Prexasertib dimesylate demonstrates significant anti-tumor activity, making it a valuable tool for cancer research and therapeutic development. -
Cyclins/Cdk Inhibitor
Aminopurvalanol A is a selective inhibitor of Cyclins/Cdk complexes, primarily targeting the G2/M-phase transition. This compound effectively inhibits cancer cell differentiation and proliferation, making it a valuable tool for cancer research. Additionally, Aminopurvalanol A has been shown to disrupt sperm fertilizing ability by inhibiting capacitation-dependent actin polymerization, highlighting its potential in reproductive biology studies. -
CDK9 Inhibitor
(-)-Enitociclib is a selective inhibitor of cyclin-dependent kinase 9 (CDK9), with demonstrated capacity to induce apoptosis in various cancer cell lines. By inhibiting CDK9, it effectively reduces phosphorylation of Ser2 in the carboxyl-terminal domain (CTD) of RNA polymerase II, leading to downregulation of critical oncogenes such as MYC and MCL1. This compound exhibits significant anti-proliferative effects against MYC-positive lymphoma and multiple myeloma cells, and shows synergistic potential when combined with therapies such as Bortezomib and Lenalidomide, making it a valuable tool in hematological cancer research. -
CDK4/6 PROTAC Degrader
PROTAC CDK4/6 degrader 1 is a dual-targeted degrader designed to selectively degrade cyclin-dependent kinases CDK4 and CDK6. With DC50 values of 10.5 nM and 2.5 nM, this compound effectively inhibits cell proliferation in Jurkat cells, demonstrating an IC50 of 0.18 μM. The compound promotes G1 phase cell cycle arrest and triggers apoptosis, making it a valuable tool for studying cancer biology and potential therapeutic applications in CDK-related malignancies. -
CDK12/CCNK Molecular Glue
NCT02 is a molecular glue degrader that targets CDK12 through the E3 ubiquitin ligase DDB1, resulting in the ubiquitination and subsequent proteasomal degradation of its partner protein CCNK. This mechanism leads to the downregulation of CDK12, inhibiting its downstream signaling pathways. NCT02 exhibits significant biological activity by inducing apoptosis in tumor cells, arresting the cell cycle, and selectively inhibiting the proliferation of colorectal cancer cells with TP53 mutations or belonging to the CMS4 molecular subtype. Additionally, NCT02 demonstrates potential in suppressing tumor growth in both in vitro and in vivo models. -
KRAS Inhibitor
KRAS inhibitor-9 is a selective inhibitor of the KRAS protein, primarily targeting KRAS G12D, G12C, and Q61H mutations with a moderate binding affinity (Kd=92 μM). This compound effectively disrupts the formation of the GTP-bound active form of KRAS, leading to subsequent inactivation of downstream signaling pathways. Biological assays demonstrate that KRAS inhibitor-9 induces G2/M cell cycle arrest and promotes apoptosis in non-small cell lung cancer (NSCLC) cells harboring KRAS mutations, while sparing normal lung cells. Its application is significant in cancer research, particularly in studying KRAS-driven malignancies. -
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).
