Catalog No.
Product Name
Application
Product Information
Citations
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EGFR inhibitor
Befotertinib (D-0316) mesylate is an orally active EGFR tyrosine kinase inhibitor that suppresses tumor cell proliferation. It is primarily investigated for its potential in treating EGFR T790M-positive non-small cell lung cancer (NSCLC). -
EGFR inhibitor
O-Desmethyl gefitinib is an active plasma metabolite of gefitinib, formed via CYP2D6-mediated metabolism. It retains EGFR inhibitory activity with an IC50 of 36 nM in subcellular assays. -
EGFR/PI3K Inhibitor
MTX-531 is an orally active small molecule that inhibits EGFR (IC50 = 14.7 nM) and multiple PI3K isoforms, with IC50 values of 6.4 nM (PI3Kα), 233 nM (PI3Kβ), 8.3 nM (PI3Kγ), and 1.1 nM (PI3Kδ), demonstrating potent antitumor activity. Additionally, MTX-531 functions as a weak PPARγ agonist (IC50 = 2.5 µM), which may mitigate PI3K inhibitor-induced hyperglycemia. -
EGFR inhibitor
Rezivertinib (BPI-7711) is an orally active, highly selective, and irreversible third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI). It is designed to potently target both common activating EGFR mutations and the resistance-associated T790M mutation, which is a frequent cause of acquired resistance to earlier-generation TKIs. Rezivertinib also demonstrates excellent central nervous system (CNS) penetration, making it effective against brain metastases in EGFR-mutant non-small cell lung cancer (NSCLC). With its strong antitumor activity and favorable pharmacokinetic profile, Rezivertinib is a promising candidate for the treatment of EGFR-mutant NSCLC, particularly in patients with CNS involvement or T790M-driven resistance. -
pan-ErbB inhibitor
Dacomitinib (PF-00299804) hydrate is an orally active, irreversible pan-ErbB inhibitor targeting EGFR, HER2, and HER4. It potently inhibits ErbB family signaling pathways, suppressing tumor proliferation and survival. Dacomitinib hydrate is a valuable agent for research into cancers, particularly metastatic non-small cell lung cancer (NSCLC), where it demonstrates efficacy in targeting EGFR-driven oncogenesis. -
EGFR inhibitor
PP 3 (Compound 3) is an EGFR tyrosine kinase inhibitor with an IC50 of 2.7 μM. It targets the EGFR signaling pathway, which is critical for cell proliferation and survival in various cancers. PP 3 is a useful tool for research into EGFR-driven malignancies, such as non-small cell lung cancer and head and neck squamous cell carcinoma, enabling studies on tumor growth inhibition and potential therapeutic strategies. -
PDGFRβ/VEGFR-2 inhibitor
Tyrphostin AG1433 (SU1433) is a tyrosine kinase inhibitor that selectively targets platelet-derived growth factor receptor beta (PDGFRβ) and vascular endothelial growth factor receptor 2 (VEGFR-2/Flk-1/KDR), with IC₅₀ values of 5.0 μM and 9.3 μM, respectively. By inhibiting these key angiogenic receptors, AG1433 disrupts downstream signaling involved in endothelial cell proliferation and migration, thereby effectively preventing blood vessel formation (angiogenesis). It is a valuable compound for research into tumor angiogenesis, vascular disorders, and anti-angiogenic therapeutic strategies. -
VEGFR2 inhibitor
VEGFR2-IN-2 (compound 6e) is a highly potent and selective inhibitor of vascular endothelial growth factor receptor 2 (VEGFR2), exhibiting an IC50 of 19.32 nM. It effectively targets VEGFR2-mediated signaling, which is critical for tumor angiogenesis, thereby inhibiting tumor growth and metastasis. VEGFR2-IN-2 is a valuable tool for research into anti-angiogenic therapies, particularly for cancers such as colorectal, breast, lung, and ovarian cancers, where VEGFR2-driven angiogenesis plays a significant role. Its high selectivity and potency make it suitable for studying VEGFR2-specific mechanisms in tumor progression and evaluating combination therapies with other targeted agents. -
VEGFR-3 inhibitor
EVT801 is an orally active, selective VEGFR-3 inhibitor (IC50=11 nM) with potent antitumor properties. It suppresses VEGF-C-induced human endothelial cell proliferation and tumor-associated lymphatic angiogenesis in mouse models. EVT801 reduces tumor hypoxia, immunosuppressive cytokines (CCL4, CCL5), and myeloid-derived suppressor cell (MDSC) production. When combined with immune checkpoint therapy (ICT), EVT801 enhances response rates and improves tumor inhibition in cancer mouse models. Additionally, EVT801 is a click chemistry reagent containing an alkyne group, enabling copper-catalyzed azide-alkyne cycloaddition (CuAAC) with azide-containing molecules. -
Aurora A/B inhibitor
Tinengotinib (TT00420) is an orally bioavailable, spectrally selective small-molecule kinase inhibitor targeting Aurora A/B (IC50=1.2–3.3 nM), FGFR1/2/3 (IC50=1.5–3.5 nM), VEGFRs, JAK1/2, and CSF1R. It disrupts Aurora kinase-mediated cell cycle progression, inducing G2/M arrest, inhibits the FGFR/JNK-JUN signaling pathway, and activates the MEK/ERK-dependent apoptotic pathway. Tinengotinib exhibits potent anti-tumor proliferation, pro-apoptotic, anti-angiogenic, and tumor microenvironment-modulating activities. It is a promising candidate for research in triple-negative breast cancer (TNBC), gallbladder cancer, and tumor immune microenvironment studies. -
FGFR inhibitor
Gunagratinib (ICP-192) is a low-toxicity, orally active, irreversible pan-FGFR inhibitor that covalently binds to fibroblast growth factor receptors (FGFR1–4), potently and selectively blocking FGFR-mediated signaling. It is designed for the treatment and study of FGFR-driven cancers, including those with FGFR alterations implicated in tumor growth and survival. -
FGFR4 inhibitor
Irpagratinib (ABSK011) is an orally active and highly potent FGFR4 (fibroblast growth factor receptor 4) inhibitor with an IC₅₀ of less than 10 nM. It effectively inhibits FGFR4 autophosphorylation, thereby blocking downstream signaling pathways critical for tumor cell survival and proliferation. Pharmacokinetic studies in mice, rats, and dogs have demonstrated high systemic exposure of Irpagratinib, supporting its potential for oral dosing in clinical applications. In preclinical models, Irpagratinib has shown significant antitumor activity, particularly in subcutaneous xenograft tumor models, making it a promising candidate for the treatment of FGFR4-driven cancers such as hepatocellular carcinoma. -
FGFR inhibitor
Resigratinib (KIN-3248) is an irreversible, orally active covalent inhibitor targeting fibroblast growth factor receptors FGFR1–4. It binds covalently to the conserved cysteine residue Cys492 within the kinase domain, effectively blocking FGFR signaling. Resigratinib demonstrates potent activity against both wild-type FGFRs and clinically relevant drug-resistant mutations, including FGFR2 V565F and FGFR3 V555M. -
FGFR2 inhibitor
Lirafugratinib (RLY-4008) is an orally active, irreversible, and highly selective inhibitor of fibroblast growth factor receptor 2 (FGFR2), with an IC₅₀ of 3 nM. It covalently binds to cysteine 491 (Cys491) in the FGFR2 kinase domain, enabling durable inhibition of FGFR2 signaling. Lirafugratinib is specifically designed to target FGFR2-driven cancers, including those with primary activating alterations and acquired resistance mutations, while sparing other FGFR family members to minimize off-target effects. It has demonstrated potent antitumor activity, including tumor regression, making it a promising therapeutic candidate for FGFR2-altered malignancies such as intrahepatic cholangiocarcinoma and other solid tumors. -
EGFR inhibitor
JBJ-09-063 hydrochloride is a highly potent, mutant-selective allosteric inhibitor of epidermal growth factor receptor (EGFR), specifically designed to target both TKI-sensitive and TKI-resistant EGFR mutations. It exhibits exceptionally low IC₅₀ values of: * 0.147 nM for EGFR L858R * 0.063 nM for EGFR L858R/T790M * 0.083 nM for EGFR L858R/T790M/C797S * 0.396 nM for EGFR^LT/L747S JBJ-09-063 hydrochloride effectively suppresses phosphorylation of EGFR and downstream signaling components, including Akt and ERK1/2, thereby inhibiting oncogenic signaling pathways. Its robust efficacy across a range of EGFR mutation profiles—including triple mutants that are resistant to third-generation TKIs—makes it a promising candidate for research and development in the treatment of EGFR-mutant non-small cell lung cancer (NSCLC). -
EGFR activator
Isoprocurcumenol is a guaiane-type sesquiterpene isolated from *Curcuma comosa* with notable bioactivity in epidermal growth factor receptor (EGFR) signaling. It activates EGFR and enhances downstream phosphorylation of ERK and AKT, key mediators of cell survival and proliferation pathways. As a result, isoprocurcumenol promotes keratinocyte proliferation, suggesting potential applications in skin regeneration, wound healing, and dermatological research. -
BMP receptor agonist
SY-LB-35 is a potent agonist of bone morphogenetic protein (BMP) receptors, capable of activating both canonical and non-canonical signaling pathways. In the C2C12 myoblast cell line, SY-LB-35 significantly enhances cell proliferation and viability, promoting cell cycle progression by increasing the proportion of cells in the S and G2/M phases. Mechanistically, it activates the canonical Smad pathway as well as non-canonical PI3K/Akt, ERK, p38, and JNK signaling cascades. These properties make SY-LB-35 a valuable tool for studying BMP-related cellular processes and a potential therapeutic candidate for tissue regeneration and muscle repair. -
EGFR degrader
MS-39 is a highly potent and selective PROTAC degrader specifically engineered to target mutant forms of the epidermal growth factor receptor (EGFR). It is constructed by conjugating the EGFR inhibitor gefitinib to a von Hippel–Lindau (VHL) E3 ligase ligand via a tailored linker. MS-39 exhibits strong binding affinity and efficient degradation of mutant EGFR proteins, offering a promising strategy for overcoming resistance in EGFR-driven cancers. Its design enables targeted proteasomal degradation rather than mere kinase inhibition, providing a novel approach to cancer therapy. -
multi-kinase PROTAC degrader
SB1-G-187 is a multifunctional PROTAC designed as a multi-kinase degrader, capable of inducing the selective degradation of multiple kinase targets through the ubiquitin–proteasome system. In addition to its targeted degradation activity, SB1-G-187 features an alkyne functional group, enabling its use as a click chemistry reagent. It can undergo copper-catalyzed azide-alkyne cycloaddition (CuAAC) with azide-containing molecules, allowing for versatile applications in chemical biology, such as probe development, conjugation, and target identification. -
PROTAC degrader
SJF-8240 (PROTAC 7) is a proteolysis-targeting chimera (PROTAC) designed to selectively degrade the receptor tyrosine kinase c-Met. It induces polyubiquitination and subsequent proteasomal degradation of c-Met, leading to effective inhibition of downstream signaling. SJF-8240 exhibits potent antiproliferative activity in GTL16 gastric cancer cells, with an IC₅₀ of 66.7 nM, making it a promising tool for targeted cancer therapy and c-Met–driven tumor research. -
IRAK4 degrader
KTX-582 is a potent heterobifunctional PROTAC degrader that targets interleukin-1 receptor–associated kinase 4 (IRAK4) and the transcription factor Ikaros, with DC₅₀ values of 4 nM and 5 nM, respectively. It induces apoptosis in MYD88^L265P-mutant diffuse large B-cell lymphoma (DLBCL) cells, a subtype characterized by constitutive IRAK4 signaling. In preclinical lymphoma models, KTX-582 effectively drives in vivo tumor regression, highlighting its therapeutic potential for MYD88-mutant hematologic malignancies. -
PROTAC EGFR degrader
MS9449 is a potent PROTAC-based degrader of the epidermal growth factor receptor (EGFR), exhibiting strong binding affinities with K\_d values of 17 nM for wild-type EGFR and 10 nM for the L858R mutant. It effectively induces degradation of mutant EGFR proteins via both the ubiquitin–proteasome system (UPS) and the autophagy–lysosome pathway, enabling dual-pathway clearance. MS9449 shows strong antiproliferative activity in non-small cell lung cancer (NSCLC) cells, making it a valuable compound for anticancer research, particularly in EGFR-driven tumors. -
Multi-target Inhibitor
Chiauranib (CS2164) is an orally active, multi-targeted small molecule inhibitor with potent anticancer activity. It targets key kinases involved in tumor angiogenesis, including VEGFR1, VEGFR2, VEGFR3, PDGFRα, and c-Kit, as well as mitosis-related kinase Aurora B and inflammation-associated kinase CSF-1R. Chiauranib exhibits IC₅₀ values ranging from 1 to 9 nM against these targets. Through simultaneous inhibition of angiogenesis, cell division, and inflammation pathways, Chiauranib exerts strong antitumor effects and is a promising candidate for the treatment of various solid tumors. -
ErbB2 inhibitor
AG-825 is a selective, ATP-competitive inhibitor of ErbB2 (HER2) tyrosine kinase, with an IC₅₀ of 0.35 μM. It exhibits both anticancer and anti-inflammatory activities and has been shown to significantly accelerate apoptosis in human neutrophils. AG-825 also increases β₁-adrenergic receptor (β₁AR) density, suggesting potential cardiomodulatory effects. Due to its multifaceted biological activity, AG-825 is a valuable compound for research in oncology, inflammation, and cardiovascular disease. -
EGFR inhibitor
Limertinib (ASK120067) is a potent and orally active third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) that selectively targets the EGFR^T790M resistance mutation with an IC₅₀ of 0.3 nM, while exhibiting reduced activity against wild-type EGFR (EGFR^WT, IC₅₀ = 6.0 nM). It is being investigated as a targeted therapy for non-small cell lung cancer (NSCLC) harboring EGFR-activating and resistance mutations. -
EGFR inhibitor
BLU-945 is a potent, highly selective, reversible, and orally bioavailable tyrosine kinase inhibitor (TKI) targeting mutant forms of the epidermal growth factor receptor (EGFR). It effectively inhibits EGFR variants harboring activating mutations such as L858R or exon 19 deletions, as well as resistance-associated mutations including T790M and C797S. BLU-945 is being developed as a next-generation therapeutic agent for the treatment of EGFR-mutant non-small cell lung cancer (NSCLC), particularly in cases resistant to earlier-generation EGFR inhibitors. -
EGFR inhibitor
CH7233163 is a noncovalent, ATP-competitive inhibitor that selectively targets the EGFR-Del19/T790M/C797S triple mutation, a known resistance mechanism to third-generation EGFR inhibitors such as Osimertinib. It effectively inhibits EGFR phosphorylation in Del19/T790M/C797S-mutant NIH3T3 cells and demonstrates significant antitumor activity in preclinical models. CH7233163 offers a promising therapeutic strategy for overcoming resistance in EGFR-mutant non-small cell lung cancer. -
ErbBs/BTK Inhibitor
Sunvozertinib (DZD9008) is a potent, orally active inhibitor of ErbB family kinases, including mutant forms of EGFR and HER2, as well as Bruton's tyrosine kinase (BTK). It demonstrates strong inhibitory activity against a range of clinically relevant EGFR mutations, with IC₅₀ values of 20.4 nM for EGFR exon 20 NPH insertion, 20.4 nM for EGFR exon 20 ASV insertion, 1.1 nM for EGFR L858R/T790M, and 7.5 nM for HER2 exon 20 YVMA mutation. It exhibits reduced activity against wild-type EGFR (IC₅₀ = 80.4 nM in A431 cells), supporting its selectivity for mutant forms. Sunvozertinib is being investigated as a targeted therapy for non-small cell lung cancers harboring EGFR or HER2 exon 20 alterations. -
EGFR inhibitor
Asandeutertinib (Osimertinib-d₃; AZD-9291-d₃) is a deuterated analog of Osimertinib, functioning as a tyrosine kinase inhibitor targeting the epidermal growth factor receptor (EGFR). It retains potent antineoplastic activity and is primarily used in research settings to study EGFR-driven cancers, particularly non-small cell lung cancer (NSCLC) with EGFR mutations, while offering potential advantages in pharmacokinetics due to deuterium substitution. -
EGFR inhibitor
(E)-AG 556 is a highly selective inhibitor of epidermal growth factor receptor (EGFR) that also exhibits anti-inflammatory activity by blocking lipopolysaccharide (LPS)-induced tumor necrosis factor-alpha (TNF-α) production. Its dual functionality makes it a valuable compound for investigating EGFR-driven signaling pathways as well as inflammation-related mechanisms. -
EGFR inhibitor
Pebezertinib (BLU-451) is an orally bioavailable epidermal growth factor receptor (EGFR) inhibitor with demonstrated central nervous system (CNS) penetration. It is specifically designed to target EGFR mutations, including exon 20 insertions, and is being investigated for the treatment of non-small cell lung cancer (NSCLC) harboring these alterations. Pebezertinib represents a promising therapeutic candidate for overcoming resistance in EGFR-driven NSCLC, particularly in cases with CNS involvement. -
TAK1 inhibitor
HS-276 is an orally bioavailable, potent, and highly selective inhibitor of transforming growth factor-β–activated kinase 1 (TAK1), with a Kᵢ of 2.5 nM. It exhibits strong inhibition of TAK1 and moderate activity against a panel of other kinases, including CLK2, GCK, ULK2, MAP4K5, IRAK1, NUAK, CSNK1G2, CAMKKβ-1, and MLK1, with respective IC₅₀ values ranging from 8.25 to 5585 nM. HS-276 is a valuable tool for investigating TAK1-mediated signaling pathways and holds therapeutic potential for inflammatory conditions such as rheumatoid arthritis (RA). -
EGFR PROTAC degrader
SJF-1521 is a selective PROTAC degrader targeting the epidermal growth factor receptor (EGFR). It incorporates lapatinib, a known EGFR inhibitor, as the targeting ligand and promotes proteasomal degradation of EGFR. SJF-1521 effectively induces EGFR degradation in OVCAR8 ovarian cancer cells, offering a promising strategy for disrupting EGFR signaling in EGFR-driven malignancies. -
PROTAC ALK/EGFR degrader
SIAIS164018 hydrochloride is a PROTAC-based dual degrader targeting ALK and EGFR, with IC₅₀ values of 2.5 nM for ALK and 6.6 nM for the ALK G1202R mutant. It effectively suppresses cancer cell migration and invasion, induces G1 phase cell cycle arrest, and promotes apoptosis, making it a promising candidate for targeted cancer therapy research. -
PROTAC EGFR degrader
MS9427 TFA is a potent PROTAC degrader targeting EGFR, with binding affinities (K_d) of 7.1 nM for wild-type EGFR and 4.3 nM for the EGFR L858R mutant. It selectively degrades the mutant EGFR via both the ubiquitin–proteasome system (UPS) and autophagy–lysosome pathways. MS9427 TFA effectively inhibits the proliferation of non-small cell lung cancer (NSCLC) cells and is a valuable tool for anticancer research focused on EGFR-driven malignancies. -
PROTAC c-Src kinase degrader
DAS-5-oCRBN is a selective and potent PROTAC degrader of c-Src kinase, acting through CRBN-mediated ubiquitination. It effectively reduces c-Src levels and inhibits proliferation in c-Src-dependent cancer cell lines, making it a useful tool for targeted protein degradation research. -
PROTAC IRAK4 degrader
PROTAC IRAK4 Degrader-1 is a cereblon-based PROTAC targeting IRAK4, derived from US patent US20190192668A1 (Compound I-210). It induces IRAK4 degradation in OCI-LY-10 cells with <20% at 0.01 μM, >20–50% at 0.1 μM, and >50% at 1 μM. -
PROTAC ALK Degrader
TL13-112 is a potent and selective PROTAC degrader targeting ALK, with an IC₅₀ of 0.14 nM for ALK inhibition. In addition to ALK, TL13-112 also induces degradation of Aurora A (IC₅₀: 8550 nM), FER (42.4 nM), PTK2 (25.4 nM), and RPS6KA1 (677 nM), supporting its utility in kinase signaling and cancer research. - PROTAC IRAK3 Degrader-1 (Compound 23) is a potent and selective PROTAC molecule targeting IRAK3, with an IC₅₀ of 5 nM. It enables efficient degradation of IRAK3, providing a valuable tool for studying innate immune signaling and inflammatory pathways.
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PROTAC IRAK4 degrader
KT-474 (SAR444656) is a selective small-molecule PROTAC degrader of IRAK4, under development for the treatment of TLR/IL-1R–mediated autoimmune diseases. It effectively suppresses R848 (TLR7/8)- and LPS-induced IL-6 and IL-8 production in peripheral blood mononuclear cells (PBMCs), highlighting its potential as an anti-inflammatory therapeutic. -
TrkA/Akt Inhibitor
HS-345 is a selective inhibitor of the TrkA/Akt signaling pathway, demonstrating significant anti-cancer effects in pancreatic cancer models. It inhibits the growth and proliferation of pancreatic cancer cells while inducing apoptosis. Moreover, HS-345 disrupts angiogenesis by downregulating the expression of HIF-1α and VEGF. This compound shows potential as a valuable tool for research into pancreatic cancer therapies. -
PI3Kα/c-Met Inhibitor
DFX117 is a selective, orally active inhibitor targeting PI3Kα and c-Met tyrosine kinase. This compound effectively inhibits the PI3K/Akt/mTOR pathway, demonstrating significant antiproliferative activity against cancer cell lines such as NCI-H1975, NCI-H1993, and HCC827, with IC50 values ranging from 0.02 to 0.08 µM. DFX117 induces cell cycle arrest at the G0/G1 phase and promotes apoptosis in A549 and NCI-H1975 cells. Additionally, DFX117 exhibits notable antitumor efficacy in murine models, making it a valuable tool for cancer research. -
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). -
IGF-1R/IR Inhibitor
GTx-134 is a dual inhibitor of insulin-like growth factor 1 receptor (IGF-1R) and insulin receptor (IR), exhibiting IC50 values of 97 nM and 187 nM, respectively. This compound effectively inhibits IGF-1R autophosphorylation and downstream Akt signaling, thereby interfering with the proliferation and survival of tumor cells. GTx-134 demonstrates broad-spectrum activity against multiple myeloma cell lines, inducing apoptosis in sensitive cells, and significantly reduces tumor growth in mouse models of myeloma. Its potential for synergistic effects with existing therapies makes GTx-134 a valuable reagent for high-risk myeloma research. -
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).
