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Catalog No.
Product Name
Application
Product Information
Citations
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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. -
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. -
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. -
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. -
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. -
KRAS G12C inhibitor
AZD4625 (Compound 21) is a highly potent, selective, covalent, and allosteric inhibitor of the mutant GTPase KRAS^G12C. It exhibits strong target engagement and high oral bioavailability, making it a promising candidate for the treatment of KRAS^G12C-driven cancers. -
KRAS G12D inhibitor
HRS-4642 is a selective KRAS^G12D inhibitor with a dissociation constant (Kd) of 0.083 nM, demonstrating potent anti-cancer activity. It synergizes with Carfilzomib and exhibits strong in vivo efficacy, promoting remodeling of the tumor microenvironment into an immune-activating state.
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RAS(ON) Inhibitor
Daraxonrasib (RMC-6236) is an orally active, non-covalent RAS(ON) inhibitor that disrupts the interaction between wild-type or mutant RAS proteins and the RAS-binding domain of BRAF. It exhibits EC₅₀ values ranging from 28 to 220 nM across wild-type KRAS, NRAS, HRAS, and multiple oncogenic RAS variants. RMC-6236 inhibits pERK signaling and demonstrates anti-tumor activity in KRAS-mutant tumor models.
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pan-KRAS Inhibitor
BI-2865 is a non-covalent pan-KRAS inhibitor that binds to wild-type and mutant KRAS variants, including G12C, G12D, G12V, and G13D, with dissociation constants (K\_D) of 6.9, 4.5, 32, 26, and 4.3 nM, respectively. It inhibits the proliferation of Ba/F3 cells expressing KRAS^G12C, KRAS^G12D, or KRAS^G12V, with a mean IC₅₀ of approximately 140 nM. -
pan-KRAS inhibitor
AMG410 is a non-covalent, selective pan-KRAS inhibitor with IC₅₀ values of 1–4 nM against KRAS^G12D, KRAS^G12V, and KRAS^G13D. It demonstrates over 100-fold selectivity against HRAS and NRAS. AMG410 functions as a dual-state inhibitor, binding both GDP-bound (K\_d = 1 nM) and GTP-bound (K\_d = 22 nM) KRAS, effectively blocking signaling independent of the nucleotide state. It also inhibits proliferation in wild-type KRAS-amplified tumor cells and is suitable for research in colorectal, pancreatic, and lung cancers. -
KRAS G12C inhibitor
Divarasib (GDC-6036) is an orally bioavailable, highly potent, and selective KRAS^G12C inhibitor with an IC₅₀ of <0.01 μM. It covalently binds to the switch II (SW-II) pocket of KRAS^G12C, irreversibly locking the protein in its inactive GDP-bound conformation. -
KRAS Switch I/II Pocket Inhibitor
BI-2852 is a KRAS inhibitor designed to target the switch I/II (SI/II) pocket with nanomolar affinity. Unlike covalent KRAS^G12C inhibitors that bind the switch II pocket, BI-2852 exhibits a distinct mechanism of action and binds preferentially to active KRAS^G12D with \~10-fold greater affinity than KRAS^WT (740 nM vs. 7.5 μM). It disrupts interactions between KRAS and GEFs, GAPs, and effectors, thereby inhibiting downstream signaling and exerting antiproliferative effects in KRAS-mutant cells. -
KRAS G12C inhibitor
Opnurasib (JDQ-443, also known as NVP-JDQ443) is an orally active, potent, selective, and covalent KRAS^G12C inhibitor, as described in patent WO2021120890A1. It exhibits strong antitumor activity in KRAS^G12C-driven cancer models. -
ULK1/2 inhibitor
DCC-3116 is an orally active inhibitor of ULK1/2 that suppresses autophagy in lung cancer cells. By targeting ULK1/2, DCC-3116 inhibits KRAS^G12C-driven signaling pathways, leading to reduced cell proliferation and demonstrating anti-tumor activity in KRAS-mutant lung cancer models. -
TrxR-1 inhibitor
Manumycin A is a polyketide antibiotic that functions as an inhibitor of thioredoxin reductase 1 (TrxR-1). It exhibits anti-tumor activity by inhibiting breast cancer cell growth, potentially through LC3-mediated mechanisms. Manumycin A also downregulates pro-inflammatory cytokine release in TNF-α-stimulated human monocytes, indicating anti-inflammatory potential. Additionally, it inhibits the Ras/Raf/ERK1/2 signaling pathway and hnRNP H1 in castration-resistant prostate cancer cells, thereby suppressing exosome biogenesis and secretion. -
RAS-G12V inhibitor
RMC-5127 is an orally active, brain-penetrant, mutant-selective tri-complex inhibitor targeting RASG12V. It non-covalently binds to cyclophilin A (CypA), forming a binary complex that engages active RASG12V to create a high-affinity tri-complex, thereby sterically blocking RAS-effector interactions. RMC-5127 inhibits RAS signaling in KRASG12V-mutant cancer cells, suppressing proliferation and inducing apoptosis. It holds promise for the study of RAS-mutant cancers, including non-small cell lung cancer. -
KRAS G12D inhibitor
MRTX1133 is a noncovalent, potent, and selective KRAS G12D inhibitor featuring an alkyne-based structure. It binds with high affinity to the switch II pocket of KRAS G12D, with an estimated KD of 0.2 pM, engaging three key substituents that enhance protein interactions. MRTX1133 inhibits SOS1-mediated nucleotide exchange and disrupts formation of the KRAS G12D/GTP/RAF1 complex, thereby blocking downstream mutant KRAS signaling. It selectively targets KRAS G12D mutant cells without affecting KRAS wild-type cells, exhibiting single-digit nanomolar potency in cellular assays and strong antitumor efficacy in KRAS G12D-driven in vivo models. -
ROCK1/2 inhibitor
DJ4 is an ATP-competitive inhibitor of ROCK1/2 and MRCKα/β, with IC₅₀ values of 5 nM and 50 nM for ROCK1 and ROCK2, and 10 nM and 100 nM for MRCKα and MRCKβ, respectively. It blocks stress fiber formation and induces apoptosis, making it a valuable compound for cancer research. -
ROCK 1/2 inhibitor
HSD1590 is a potent inhibitor of Rho-associated protein kinases, with IC₅₀ values of 1.22 nM for ROCK1 and 0.51 nM for ROCK2. It exhibits strong binding affinity to ROCK isoforms (K\_d < 2 nM) and demonstrates low cytotoxicity, making it suitable for further research applications. -
PKC isoenzymes inhibitor
CRT0066854 is a potent and selective inhibitor of atypical protein kinase C (PKC) isoenzymes. It inhibits full-length PKCι, PKCζ, and ROCK-II with IC₅₀ values of 132 nM, 639 nM, and 620 nM, respectively. -
ROCK inhibitor
AS1892802 is a potent, orally active, and highly selective inhibitor of Rho-associated kinase (ROCK). It exhibits a rapid onset of antinociceptive effect, comparable to that of Tramadol and Diclofenac. Unlike traditional analgesics, AS1892802 does not induce gastric irritation or abnormal behavior, making it a promising candidate for research in the treatment of severe osteoarthritis pain. -
ROCK inhibitor
PF-4950834 is a potent, selective, and orally bioavailable ATP-competitive inhibitor of Rho-associated kinases, with IC₅₀ values of 8.35 nM for ROCK2 and 33.12 nM for ROCK1. It effectively inhibits neutrophil migration and is suitable for research on inflammation and immune cell regulation. -
ROCK inhibitor
OXA-06 hydrochloride is an ATP-competitive inhibitor of Rho-associated protein kinase (ROCK) that suppresses anchorage-dependent growth and invasion of non-small cell lung cancer (NSCLC) cell lines. It inhibits cofilin phosphorylation without inducing apoptosis. -
Kinases PROTAC/Nek9 Inhibitor
DB0614 is a PROTAC molecule utilizing a cereblon ligand, designed as a selective and potent degrader of NEK9 and other kinases. It induces the degradation of multiple kinases, including ABL1, ABL2, BLK, CDK11B, CDK4, CSK, EPHA3, FER, GAK, LIMK1, MAP3K20, MAP4K1–3, MAP4K5, MAPK14, MAPK7–9, MAPKAPK2/3, NLK, PDIK1L, PTK2B, RIPK1, RPS6KA1/3, SIK2/3, STK35, TNK2, and ULK1. DB0614 is suitable for research involving diseases or disorders driven by aberrant kinase activity. -
CDK inhibitor
(R)-CR8 is a second-generation analog of Roscovitine and a potent inhibitor of CDK1, CDK2, CDK5, CDK7, and CDK9. It inhibits CDK1/cyclin B (IC₅₀ = 0.09 μM), CDK2/cyclin A (0.072 μM), CDK2/cyclin E (0.041 μM), CDK5/p25 (0.11 μM), CDK7/cyclin H (1.1 μM), CDK9/cyclin T (0.18 μM), and CK1δ/ε (0.4 μM). (R)-CR8 induces apoptosis, exhibits neuroprotective effects, and functions as a molecular glue degrader that promotes the degradation of cyclin K. -
CDK4/6 inhibitor
Culmerciclib (TQB3616) is a potent cyclin-dependent kinase (CDK)4/6 inhibitor with strong antineoplastic activity. It demonstrates significant synergistic antitumor effects in estrogen receptor (ER)-positive/HER2-negative and HER2-positive breast cancer models when combined with endocrine therapy or HER2-targeted treatments, supporting its potential for combination cancer therapy. -
CDK7 Inhibitor
SY-5609 (CDK7-IN-3) is an orally active, highly selective, and noncovalent inhibitor of CDK7, with a Kd of 0.065 nM. It demonstrates minimal activity against CDK2 (Ki = 2600 nM), CDK9 (Ki = 960 nM), and CDK12 (Ki = 870 nM), confirming its selectivity. SY-5609 induces apoptosis in tumor cells and exhibits potent antitumor activity, making it a promising candidate for targeted cancer therapy. -
CDK5 inhibitor
CP681301 is a potent CDK5 inhibitor with demonstrated antiproliferative activity. It reduces the expression of key stemness and proliferation markers—including CD133, OLIG2, SOX2, KI67, and phosphorylated CDK5—in glioma stem cells (GSCs). CP681301 also impairs self-renewal capacity in mouse glioma xenograft models and exhibits anti-tumor activity in *Drosophila*, making it a promising compound for glioma and cancer stem cell research.
