Catalog No.
Product Name
Application
Product Information
Citations
-
KRAS degrader
ACBI3 is a PROTAC designed to target KRAS, employing a unique mechanism to induce degradation of this oncogenic protein. It comprises a pan-KRAS degrader linked to an E3 ligase ligand through a specialized linker, facilitating the recruitment of the proteasome for degradation. ACBI3 has demonstrated significant biological activity by achieving durable modulation of signaling pathways and promoting tumor regression in KRAS mutant xenograft mouse models, making it a valuable tool for research into cancer therapeutics aimed at KRAS-driven malignancies. -
PROTAC AURORA-A Degrader
JB170 is a potent PROTAC-mediated degrader targeting AURORA-A kinase, with a DC50 of 28 nM. By conjugating Alisertib with the Cereblon-binding molecule Thalidomide, JB170 selectively binds AURORA-A (EC50=193 nM) over AURORA-B (EC50=1.4 µM). The compound induces S-phase cell cycle arrest specifically via the depletion of AURORA-A and effectively inhibits its non-catalytic functions. JB170 serves as a valuable tool for studying AURORA-A's roles in cellular processes and therapeutic applications in cancer research. -
PROTAC CDK6 Degrader
CP-10 is a PROTAC designed to selectively target and degrade cyclin-dependent kinase 6 (CDK6) through its binding to Cereblon. Demonstrating a DC50 of 2.1 nM, this compound effectively inhibits the proliferation of various hematopoietic cancer cell lines, including multiple myeloma, and is capable of degrading both mutated and overexpressed forms of CDK6. Its specific activity makes CP-10 a valuable tool for research into CDK6-related malignancies and potential therapeutic strategies. -
PROTAC KRAS G12D Degrader
PROTAC KRAS G12D degrader 1 functions as a selective PROTAC targeting the KRAS G12D mutant by promoting its degradation. This compound effectively inhibits the proliferation of KRAS G12D-mutant cell lines and suppresses phosphorylation of ERK, a critical pathway in cancer signaling. In vivo studies demonstrate its ability to impede tumor growth in mice with AsPC-1 xenografts, making it a valuable tool for research into KRAS G12D-driven cancers. -
SOS1 Inhibitor
SOS1-IN-14 is a potent and selective inhibitor of SOS1, demonstrating an IC50 value of 3.9 nM. This orally active compound is absorbed in the intestine through a P-glycoprotein-mediated efflux mechanism. SOS1-IN-14 is primarily utilized in research on KRAS-mutated cancers, showcasing superior tumor suppression capabilities compared to alternative therapies. -
Rac1 Inhibitor
Rac1-IN-4 is a selective inhibitor of Rac1, a Rho GTPase involved in various cellular processes including cytoskeletal dynamics and cell migration. This compound effectively disrupts the signaling pathways mediated by Rac1, making it a valuable tool for studying cancer metastasis and neurodegenerative diseases. Rac1-IN-4 is utilized in research to explore the therapeutic potential of targeting Rac1 in cellular signaling and pathology. -
Ras Inhibitor
ASP2453 is a selective and orally bioavailable inhibitor targeting the KRAS G12C mutation. It functions by inhibiting the interaction between KRAS G12C and Raf mediated by Son of Sevenless (SOS), demonstrating an IC50 value of 40 nM. ASP2453 shows potential in cancer research, particularly in studies addressing KRAS-driven malignancies. -
K-Ras Inhibitor
KRpep-2d is a potent inhibitor of K-Ras, targeting the K-Ras signaling pathway known for its role in various cancers. This compound effectively reduces the proliferation of K-Ras-driven cancer cells, making it a valuable tool for cancer research. Its application can aid in the development of therapeutic strategies for K-Ras-associated malignancies. -
SOS1/KRAS Inhibitor
SAH-SOS1A TFA is a peptide-based inhibitor targeting the SOS1-KRAS protein interaction. It exhibits nanomolar affinity for both wild-type and various mutant KRAS forms, including G12D, G12V, G12C, G12S, and Q61H (EC50 = 106-175 nM). By directly disrupting nucleotide association, SAH-SOS1A TFA effectively impairs KRAS-driven cancer cell viability and inhibits the downstream ERK-MAPK phosphosignaling cascade, making it a valuable tool for research in cancer biology. -
SOS1 Inhibitor
SOS1-IN-15 is a potent SOS1 inhibitor with an IC50 value of 5 nM, designed to specifically target and inhibit SOS1 activity. Its strong inhibitory effect makes it a promising candidate for research into KRAS-driven cancers, facilitating the understanding of oncogenic signaling pathways and development of targeted therapeutic strategies. -
Anticancer Agent
ARN22089 is a novel trisubstituted pyrimidine that acts as an anticancer agent by inhibiting the interaction of CDC42 GTPases with downstream effectors. This mechanism disrupts critical signaling pathways involved in tumorigenesis. In preclinical studies, ARN22089 has demonstrated the ability to inhibit tumor growth in a BRAF mutant mouse melanoma model, making it a valuable compound for research in cancer therapeutics and signaling pathways. -
KRASG12C Inhibitor
RM-018 is a potent KRASG12C inhibitor that specifically targets the GTP-bound, active state of KRASG12C. This tricomplex compound effectively inhibits KRASG12C/Y96D, showcasing its potential to overcome resistance mechanisms. RM-018 is an invaluable tool for studying KRAS-related signaling pathways and developing targeted therapies in cancer research. -
NRAS Proto-oncogene Expression Reducer
RGB-1 is a selective RNA G-quadruplex stabilizer that targets and reduces the expression of the NRAS proto-oncogene within breast cancer cells. This compound serves as a valuable tool for exploring the cellular mechanisms and functions of RNA G-quadruplex structures, while also aiding in the identification of novel mRNA sequences capable of forming G-quadruplexes. RGB-1 is particularly relevant for research focused on breast cancer therapeutics and the molecular basis of oncogene regulation. -
Ras Activator
Methylophiopogonanone B is a homoisoflavonoid that serves as a Ras activator. Isolated from the root of Ophiopogon japonicus, it exhibits potent antioxidant properties. This compound enhances GTP-Rho levels and activates the Rho signaling pathway, thereby inducing morphological changes in cells, such as actin cytoskeletal reorganization, dendrite retraction, and stress fiber formation. It is a valuable reagent for research into cellular signaling and structural dynamics. -
Rac1/Cdc42 Inhibitor
AZA1 is a potent dual inhibitor of Rac1 and Cdc42, key regulators of cell signaling pathways. This compound has been shown to induce apoptosis in prostate cancer cells while simultaneously inhibiting their proliferation, migration, and invasion. AZA1 serves as a valuable tool for research into the molecular mechanisms of prostate cancer progression and potential therapeutic interventions. -
Cdc42 Inhibitor
MLS-573151 is a selective inhibitor of the GTPase Cdc42, exhibiting an EC50 of 2 μM. It specifically targets Cdc42 without affecting other members of the GTPase family, such as Rab2, Rab7, H-Ras, Rac1, Rac2, and wild-type RhoA. By inhibiting GTP binding to Cdc42, MLS-573151 serves as a valuable tool for studying cellular processes regulated by this signaling pathway. Its application is essential in research related to cancer and other diseases where Cdc42 plays a critical role in cell migration and proliferation. -
Rac1 Inhibitor
Z62954982 is a selective Rac1 inhibitor with an IC50 of 12 μM, demonstrating notable potency in disrupting the Rac1/Tiam1 complex. This compound effectively reduces active Rac1 levels (GTP-bound) in the cytoplasm while preserving the function of other Rho GTPases such as Cdc42 and RhoA. Z62954982 serves as a valuable tool for studies investigating Rac1-mediated signaling pathways and their role in various biological processes. -
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. -
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.
-
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.
