Catalog No.
Product Name
Application
Product Information
Citations
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BCR-ABL PROTAC Degrader
SIAIS100 TFA is a potent PROTAC degrader targeting BCR-ABL, with a DC₅₀ of 2.7 nM. It is a valuable tool for studying BCR-ABL signaling and therapeutic strategies in chronic myeloid leukemia (CML). -
BTK degrader
NX-5948 (BTK-IN-24) is an orally bioavailable, blood-brain barrier-penetrant PROTAC degrader targeting Bruton's tyrosine kinase (BTK). It induces BTK degradation via the cereblon E3 ligase pathway, effectively inhibiting B cell activation. NX-5948 exhibits both anti-inflammatory and antitumor activities, supporting its use in cancer and immune-related research. -
BTK Inhibitor
Zelebrudomide (NX-2127) is a novel, potent BTK degrader that induces proteasomal degradation through targeted ubiquitination, rather than direct inhibition. In addition to degrading BTK, Zelebrudomide (NX-2127) enhances immune responses by stimulating T cell activation and increasing IL-2 production in primary human T cells, supporting its potential in cancer and immunotherapy research.
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ALK Inhibitor
ALK/PI3K/AKT-IN-1 is a selective ALK inhibitor that demonstrates significant anti-proliferative effects on A549, H1975, and PC9 cancer cell lines with IC50 values of 0.44, 0.83, and 1.51 μM, respectively. This compound induces cell cycle arrest at the G1 phase by enhancing p21 and p27 expression while inhibiting CDK2 and phosphorylated Rb activity. Additionally, ALK/PI3K/AKT-IN-1 disrupts the ALK/PI3K/AKT signaling pathway, leading to mitochondrial membrane depolarization and apoptosis in A549 cells. It also effectively inhibits spheroid formation and growth in A549 cells, making it a valuable tool for cancer research. -
FLT3 Inhibitor
FLT3-IN-32 hydrochloride is a potent and orally bioavailable inhibitor of FLT3, demonstrating IC50 values of 0.29 nM, 0.77 nM, and 2.07 nM against the FLT3-ITD, FLT3-D835Y, and FLT3-N676K mutations, respectively. This compound effectively reduces FLT3 phosphorylation and inhibits downstream signaling pathways such as STAT5, MAPK, and AKT, ultimately leading to apoptosis in FLT3-mutated Ba/F3 cells. Additionally, FLT3-IN-32 hydrochloride exhibits significant anti-tumor efficacy in the MV4-11 xenograft model, making it a valuable tool for investigations into acute myeloid leukemia (AML). -
FAK Inhibitor
FAK Inhibitor 7 is a potent focal adhesion kinase (FAK) inhibitor with an IC50 of 3.58 nM. This compound disrupts downstream signaling pathways associated with FAK, including Src and AKT, leading to cell cycle arrest in the G0/G1 phase and promoting cytotoxic autophagy in ovarian cancer cells. Additionally, FAK Inhibitor 7 has demonstrated efficacy in inhibiting tumor metastasis and growth in preclinical ovarian cancer mouse models, making it a valuable tool for studying cancer biology and therapeutic interventions. -
EGFR Inhibitor
WB-308 is a small molecule EGFR inhibitor, designed to target the epidermal growth factor receptor and its associated signaling pathways. In vitro studies demonstrate that WB-308 effectively reduces the proliferation and clonogenicity of non-small cell lung cancer (NSCLC) cells, leading to G2/M phase arrest and apoptosis. Additionally, it demonstrates tumor growth inhibition in both lung orthotopic transplantation and patient-derived xenograft models. WB-308 was shown to impair the phosphorylation of EGFR, AKT, and ERK1/2 proteins, offering a promising alternative to existing EGFR-targeted therapies with potentially lower cytotoxicity. -
ALK Inhibitor
ALK-IN-31 is an orally active inhibitor of anaplastic lymphoma kinase (ALK), with an IC50 of 1135 nM. This compound demonstrates significant antiproliferative activity against H2228 lung cancer cells, showing an IC50 of 1.35 μM. ALK-IN-31 induces apoptosis and halts cell cycle progression in the G0/G1 phase by modulating mitochondrial function. Furthermore, it attenuates tumor growth by downregulating p-AKT and p-mTOR within the PI3K-AKT-mTOR signaling pathway, making it a valuable tool for research in non-small cell lung cancer (NSCLC). -
VEGFR-2 Inhibitor
VEGFR-2-IN-77 is a selective inhibitor of Vascular Endothelial Growth Factor Receptor 2 (VEGFR-2), displaying an IC50 value of 139 nM. This compound effectively disrupts the PI3K/AKT/mTOR signaling pathway, leading to cytotoxic effects specifically in leukemia and prostate cancer cells. VEGFR-2-IN-77 induces cell cycle arrest and apoptosis while inhibiting cell migration and invasion. It serves as a valuable tool for investigating therapeutic strategies in leukemia and prostate cancer research. -
Dual COX-2/EGFR Inhibitor
Melafolone is a potent dual inhibitor of COX-2 and EGFR, displaying IC50 values of 13.2 μM for COX-2 and 17.4 μM for EGFR. This compound enhances the efficacy of anti-PD-1 therapy by promoting vascular normalization and downregulating PD-L1 through the PI3K/Akt signaling pathway in Lewis lung carcinoma (LLC) and CMT167 models. Melafolone is suitable for applications in lung cancer research. -
EGFR Mutant Inhibitor
EGFR-IN-176 is an orally active, ATP-competitive inhibitor specifically targeting mutant forms of the epidermal growth factor receptor (EGFR), notably the C797S-mediated triple mutant. This compound effectively suppresses AKT signaling pathways and induces apoptosis in Ba/F3 and PC-9 cell lines expressing the EGFR mutations EGFR19del/T790M/C797S and EGFRL858R/T790M/C797S. Selectivity is demonstrated by its lack of inhibition against wild-type EGFR-expressing A431 cells. Additionally, EGFR-IN-176 inhibits ALK enzymatic activity with an IC50 of less than 0.5 nM and serves as a valuable tool for research in non-small cell lung cancer (NSCLC). -
EGFR/HER2 Inhibitor
KU004 is a potent dual inhibitor of the epidermal growth factor receptor (EGFR) and human epidermal growth factor receptor 2 (HER2), exhibiting significant anticancer properties. This quinazoline derivative effectively inhibits the proliferation of human breast cancer SKBR3 cells through the induction of G1 phase cell cycle arrest. KU004 interferes with HER2 and EGFR activation, subsequently blocking downstream signaling pathways such as Akt and Erk, and promotes apoptosis primarily via the extrinsic pathway. Its mechanism makes it a valuable tool for cancer research, particularly in studies targeting breast cancer therapy. -
BTK Inhibitor
PLS-123 is a covalent, irreversible inhibitor of Bruton's tyrosine kinase (BTK), displaying an IC50 of less than 5 nM. It effectively disrupts BTK's catalytic activity at Tyr551 and self-activation at Tyr223, leading to the inhibition of key signaling pathways, including AKT/mTOR and MAPK, as well as blocking PLCγ2 activation. PLS-123 exhibits potent anti-proliferative effects against a range of B-cell lymphoma cell lines, inducing apoptosis through a caspase-dependent mechanism. Additionally, it demonstrates substantial antitumor efficacy in the OCI-Ly7 xenograft model, making it a valuable tool for research in lymphoma. -
PROTAC HIF-1α Degrader
PROTAC HIF-1α Degrader-2 is a selective degrader that targets HIF-1α, facilitating its degradation through the ubiquitin-proteasome pathway by promoting the formation of a HIF-1α/VHL ternary complex. This compound has been shown to inhibit the proliferation, migration, and colony formation of HeLa cells while also inducing apoptosis. Moreover, PROTAC HIF-1α Degrader-2 decreases the expression of p-MEK and p-AKT within the MAPK and PI3K/AKT signaling pathways, making it a valuable tool for research into cervical cancer. -
EGFR Inhibitor
EGFR kinase-IN-8 is a potent inhibitor of the epidermal growth factor receptor (EGFR), demonstrating strong inhibitory activity against both triple-mutated EGFR (L858R/T790M/C797S) and double-mutated EGFR (L858R/T790M), with IC50 values of 3.86 nM and 1.23 nM, respectively. This compound effectively suppresses EGFR phosphorylation, leading to inhibition of downstream signaling pathways, including AKT, STAT3, and MAPK. EGFR kinase-IN-8 has shown promising anticancer efficacy, particularly in the treatment of non-small cell lung cancer. -
EGFR/HER2 Inhibitor
Afatinib oxalate is a potent and irreversible dual specificity inhibitor of the ErbB family, specifically targeting EGFR and HER2. With IC50 values of 0.5 nM for EGFR wild-type, 0.4 nM for EGFR L858R, 10 nM for EGFR L858R/T790M, and 14 nM for HER2, it demonstrates strong inhibitory activity. This compound is primarily utilized in research on esophageal squamous cell carcinoma (ESCC), non-small cell lung cancer (NSCLC), and gastric cancer, making it valuable for studies focused on these malignancies. -
EGFR Inhibitor
Lazertinib mesylate hydrate is a selective, irreversible inhibitor of the epidermal growth factor receptor (EGFR) tyrosine kinase. It demonstrates high potency against both activating mutations and the T790M resistance mutation, effectively inhibiting the phosphorylation of EGFR, AKT, and ERK pathways. This compound induces apoptosis and suppresses tumor growth, particularly in non-small cell lung cancer models, making it valuable for research on brain metastases and targeted cancer therapies. -
EGFR Kinase Inhibitor
EGFR-IN-113 is an EGFR kinase inhibitor with an IC50 of 14.79 μM, effectively targeting the EGFR pathway. This compound induces apoptosis and inhibits cell proliferation through the downregulation of Akt and Erk1/2 signaling pathways. EGFR-IN-113 is suitable for research applications focused on EGFR-driven cancers, including lung, pancreatic, and breast carcinoma. -
FAK Inhibitor
FAK-IN-22 is a selective inhibitor of focal adhesion kinase (FAK) with additional activity against JAK3 and Aurora B, exhibiting IC50 values of 50.94 nM, 9.99 nM, and 0.49 nM, respectively. This compound demonstrates significant anti-tumor effects in pancreatic ductal adenocarcinoma (PDAC) by inhibiting cell proliferation, inducing apoptosis, and causing G2/M phase arrest in PANC-1 cells, with an IC50 of 0.15 μM. FAK-IN-22’s action is primarily mediated through the inhibition of the FAK/PI3K/Akt signaling pathway, making it a valuable tool for studying cancer cell dynamics and signaling mechanisms. -
FLT3 Inhibitor
FLT3-IN-34 is a selective FLT3 inhibitor, exhibiting an IC50 value of 1.4 nM. It effectively blocks FLT3 phosphorylation and disrupts downstream signaling pathways involving AKT and ERK1/2. FLT3-IN-34 induces a concentration-dependent G0/G1 phase arrest and promotes mild apoptosis in FLT3-ITD-positive MV4-11 cells, demonstrating potent anti-proliferative effects with IC50 values of 14.95 nM and 18.5 nM against MV4-11 and MOLM-13 cell lines, respectively. This compound is suitable for investigating FLT3-positive acute myeloid leukemia (AML) and understanding FLT3-related signaling mechanisms. -
T315I Mutant Bcr-Abl Inhibitor
DB07107 is a potent inhibitor of the T315I mutant Bcr-Abl tyrosine kinase, demonstrating resistance against this specific mutation associated with chronic myeloid leukemia. Additionally, DB07107 effectively inhibits Akt1 with an IC50 value of 360 nM, highlighting its dual-targeting capability. This compound is suitable for research applications related to cancer signaling pathways and the development of targeted therapies for resistant forms of leukemia. -
EGFR Inhibitor
BI-4732 is a potent, orally active EGFR inhibitor that functions through reversible, ATP-competitive mechanisms. It selectively inhibits the kinase activity of mutant EGFR variants, including L858R, T790M, and C797S, with IC50 values of 1 nM, while sparing the wild-type EGFR. Furthermore, BI-4732 effectively reduces the phosphorylation of key signaling proteins such as AKT, ERK, and S6K. Its robust intracranial anti-tumor efficacy has been demonstrated in the YU-1097 xenograft model that harbors the EGFR_E19del/T790M/C797S mutation, making it a valuable tool for research in non-small cell lung cancer (NSCLC). -
EGFR Inhibitor
BAY 2476568 is a highly selective inhibitor of EGFR targeting exon 20 insertion variants. It demonstrates potent inhibition of the kinase activity of various EGFR exon 20 mutants, including insASV, insSVD, and insNPG, with IC50 values of 0.09 nM, 0.21 nM, and 0.11 nM, respectively. BAY 2476568 effectively reduces phosphorylation of EGFR (Y1068), ERK1/2, and Akt (S473) in Ba/F3 cells harboring these mutations. This compound is valuable for investigating non-small cell lung cancer (NSCLC) associated with EGFR exon 20 insertion mutations. -
EGFR Inhibitor
Lazertinib mesylate is a selective, irreversible inhibitor of the EGFR tyrosine kinase, designed for oral administration and capable of penetrating the central nervous system. It demonstrates high efficacy against both activating mutations and the T790M resistance mutation in EGFR. By inhibiting the phosphorylation of EGFR, AKT, and ERK, Lazertinib mesylate induces apoptosis and hampers tumor growth, as evidenced in mouse models of brain metastases. This compound is primarily utilized in research investigating non-small cell lung cancer. -
FLT3-ITD Inhibitor
Clifutinib is a selective inhibitor of the FLT3-ITD mutation, exhibiting an IC50 of 15.1 nM. This compound demonstrates potent antiproliferative effects against FLT3-ITD acute myeloid leukemia (AML) cell lines, with IC50 values of 1.5 nM and 1.4 nM for MV-4-11 and MOLM-13, respectively. Clifutinib disrupts FLT3-ITD kinase activity, subsequently inhibiting downstream RAS/MAPK, PI3K/AKT, and JAK/STAT5 signaling pathways, leading to apoptosis in FLT3-ITD-positive AML cells. Additionally, it shows significant antitumor efficacy in mouse models bearing MV-4-11 or MOLM-13 xenografts, making it a valuable tool for investigating relapsed/refractory FLT3-ITD-positive AML. -
EGFR Inhibitor
Delphinidin 3-glucoside chloride is an EGFR inhibitor known for its role in inducing apoptosis in B cell chronic lymphocytic leukaemia (B CLL). It demonstrates phytoestrogen activity by selectively binding to estrogen receptor beta (ERβ) with an IC50 of 9.7 μM and inhibits EGFR with an IC50 of 2.37 µM. Additionally, Delphinidin 3-glucoside chloride exerts antitumor effects through the pAKT/IRF1/HOTAIR pathway and provides protection against oxidative stress, as well as inhibiting platelet activation and endothelial dysfunction. This compound is useful in cancer research and studies related to hormonal regulation. -
BTK Inhibitor
TL-895 is a potent, orally bioavailable, irreversible inhibitor of Bruton's tyrosine kinase (BTK) that functions as an ATP-competitive agent. It demonstrates high selectivity with an average IC50 of 1.5 nM against recombinant BTK and minimal activity against BLK, BMX, and TXK. TL-895 effectively inhibits BTK auto-phosphorylation at the Y223 site (IC50: 1-10 nM) and suppresses the production of inflammatory cytokines such as IL-8, IL-1β, MCP-1, and TNF-α in monocytes and macrophages. This compound is valuable for investigating chronic lymphocytic leukemia (CLL), myelofibrosis (MF), and various B-cell malignancies. -
ErbB-2/EGFR Inhibitor
Lapatinib ditosylate monohydrate is a selective inhibitor of the ErbB-2 and EGFR tyrosine kinase domains. It demonstrates potent biological activity with IC50 values of 10.2 nM against EGFR and 9.8 nM against ErbB-2. This compound is commonly utilized in cancer research to investigate mechanisms of tumor growth and resistance, particularly in breast cancer models. -
VEGFR-2/DHFR Inhibitor
VEGFR-2/DHFR-IN-2 is a dual inhibitor of Vascular Endothelial Growth Factor Receptor 2 (VEGFR-2) and Dihydrofolate Reductase (DHFR), exhibiting IC50 values of 0.623 μM and 9.085 μM, respectively. This compound demonstrates significant cytotoxic activity against various cancer cell lines, including C26, HepG2, and MCF7, with IC50 values ranging from 3.59 to 8.38 μM. VEGFR-2/DHFR-IN-2 is pertinent for research applications focused on cancer therapeutics and targeted inhibition of tumor angiogenesis. -
VEGFR-2/DHFR Inhibitor
VEGFR-2/DHFR-IN-1 is a dual inhibitor of VEGFR-2 and dihydrofolate reductase (DHFR), exhibiting IC50 values of 0.384 μM and 7.881 μM, respectively. This compound demonstrates significant antibacterial activity against various strains, including Escherichia coli and MRSA, with MIC values ranging from 8 to 16 μg/mL. Additionally, VEGFR-2/DHFR-IN-1 shows potent cytotoxic effects on cancer cell lines C26, HepG2, and MCF7, with IC50 values between 2.97 and 7.12 μM. This reagent is applicable for research exploring cancer therapeutics and microbial resistance. -
HIF-1α/EZH2 Inhibitor
DYB-03 is an orally active inhibitor of HIF-1α and EZH2. It effectively suppresses migration, invasion, and angiogenesis in lung cancer cells as well as human umbilical vein endothelial cells (HUVECs), demonstrated both in vitro and in vivo. Additionally, DYB-03 induces apoptosis in A549 and H460 cells that are resistant to 2-ME2 and GSK126, highlighting its potential in overcoming resistance in lung cancer therapies. -
TrxR/EGFR Inhibitor
TrxR/EGFR-IN-1 is a potent inhibitor targeting both Thioredoxin Reductase (TrxR) and Epidermal Growth Factor Receptor (EGFR). This compound demonstrates significant anti-proliferative effects against Gefitinib-sensitive and resistant lung cancer cells, facilitating apoptosis and tumor cell death. TrxR/EGFR-IN-1 promotes GPX4 protein degradation via autophagolysosomal and proteasomal pathways, leading to ferroptosis. Additionally, it induces endoplasmic reticulum stress and triggers immunogenic cell death, making it a valuable tool for studying mechanisms underlying Gefitinib-resistant lung cancer. -
ErbB-2/EGFR Inhibitor
Lapatinib tosylate is a potent inhibitor targeting the ErbB-2 and EGFR tyrosine kinase domains. With IC50 values of 10.2 nM for EGFR and 9.8 nM for ErbB-2, it effectively blocks signaling pathways associated with cell proliferation and survival. This compound is primarily utilized in cancer research and therapeutic studies, particularly for conditions driven by aberrant ErbB signaling. - Gramicidin A is a peptide component of gramicidin, an antibiotic mixture originally isolated from B. brevis. Gramicidin A is a highly hydrophobic channel-forming ionophore that forms channels in model membranes that are permeable to monovalent cations. Gramicidin A induces degradation of hypoxia inducible factor 1 α (HIF-1α).
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FGFR3 inhibitor
VSPPLTLGQLLS is a small peptide FGFR3 inhibitor, peptide P3, inhibits FGFR3 phosphorylation. VSPPLTLGQLLS inhibits 9-cisRA-induced tracheal lymphangiogenesis and blocks lymphatic endothelial cell (LEC) proliferation, migration, and tubule formation. -
Pan-PPAR Agonist, HIF-1α Inhibitor
Bavachinin is a pan-peroxisome proliferator-activated receptor (PPAR) agonist and a HIF-1α inhibitor, demonstrating IC50 values of 21.043 μM, 12.819 μM, and 0.622 μM for PPAR-α, PPAR-β/δ, and PPAR-γ, respectively. This compound exhibits significant antitumor activity against non-small cell lung cancer through its modulation of PPAR-γ. Additionally, Bavachinin possesses notable anti-inflammatory and anti-angiogenic properties, making it a valuable tool for research in cancer and metabolic disorders. Its oral bioavailability further supports its utility in various biological studies. -
HIF-PHDs Inhibitor
Adaptaquin is a blood-brain barrier (BBB)-penetrable inhibitor of hypoxia-inducible factor prolyl hydroxylases (HIF-PHDs). It exhibits anti-inflammatory and neuroprotective properties, effectively inhibiting lipid peroxidation and preserving mitochondrial function while reducing neuronal cell death. Adaptaquin is a valuable research tool for studying neurological disorders, including Parkinson's disease. -
HIF-1 Inhibitor
Moracin O is a selective inhibitor of hypoxia-inducible factor-1 (HIF-1) derived from Morus alba Linn. It demonstrates significant in vitro activity in inhibiting HIF-1, effectively reducing reactive oxygen species (ROS) production induced by oxygen-glucose deprivation (OGD). This compound is valuable for research into neuroprotection and anti-inflammatory effects, making it suitable for studies on cellular responses to hypoxic conditions. -
ROS/HIF-1α Inhibitor
Terpestacin is a potent inhibitor of reactive oxygen species (ROS) production and a negative regulator of hypoxia-inducible factor 1-alpha (HIF-1α). Derived from Phoma exigua var. heteromorpha, Terpestacin binds to UQCRB, effectively impeding mitochondrial ROS generation. Its demonstrated ability to inhibit tumor angiogenesis in the FM3A breast cancer cell xenograft model highlights its relevance in cancer research, while also exhibiting notable antitumor and phytotoxic activities. -
HIF1-α Inhibitor
Oltipraz metabolite M2 is an active metabolite that serves as a HIF-1α inhibitor. It enhances mitochondrial fuel oxidation and inhibits lipogenesis in the liver by activating AMPK, particularly in high-fat diet-fed mouse models. This compound is valuable for research focused on hepatic steatosis and steatohepatitis. -
ALK Inhibitor
Alectinib (CH5424802) is a potent, selective, and orally available ALK inhibitor with a unique chemical scaffold, showing preferential antitumor activity against cancers with gene alterations of ALK.
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Aurora A/B Kinase inhibitor
PF-03814735 is a novel, potent and reversible inhibitor of Aurora A/B with IC50of 0.8 nM/5 nM, is less potent to Flt3, FAK, TrkA, and minimally active to Met and FGFR1. Phase 1. -
EGFR Inhibitor
BMS 599626 is an orally bioavailable inhibitor of the HER1, HER2 and HER4 tyrosine kinases (IC50=22, 32 and 190 nM, respectively) with potential antineoplastic activity. -
HER2/EGFR inhibitor
TAK-285 is an investigational HER2/EGFR inhibitor that penetrates the CNS in Rats with an Intact Blood Brain Barrier (BBB). TAK-285 has inhibitory activity against HER2 and EGFR kinases with IC50 values for HER2 and EGFR of 17 nmol/L (95% CI 12-24) and 23 nmol/L (95% CI 18-30), respectively.[1]
