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Catalog No.
Product Name
Application
Product Information
Citations
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PAK1 Inhibitor
AK963/40708899 is a selective inhibitor of PAK1, disrupting the PAK1-NF-κB-cyclinB1 signaling pathway. This compound effectively suppresses the proliferation of human gastric cancer cells and induces G2 phase cell cycle arrest, consequently reducing migration and invasion. Additionally, AK963/40708899 inhibits filopodia formation and enhances cell adhesion, negatively regulating the PAK1-LIMK-cofilin and PAK1-ERK-FAK pathways, thereby diminishing the invasive potential of gastric cancer cells. This reagent is valuable for research into cancer biology and therapeutic interventions targeting PAK1 signaling pathways. -
MARCKS Inhibitor
BIO-11006 is a specific inhibitor of the MARCKS protein, known for its role in modulating inflammatory responses. This peptide attenuates lipopolysaccharide (LPS)-induced neutrophil influx into lung tissues, suppresses NF-κB activation, and reduces the expression of proinflammatory cytokines such as KC and TNF-α. BIO-11006 has demonstrated efficacy in reversing disease progression in an LPS-induced mouse model of lung injury, making it a valuable tool for research into acute lung injury and acute respiratory distress syndrome (ALI/ARDS). -
NF-κB Inhibitor
Demethyleneberberine chloride is an NF-κB inhibitor that exhibits significant anti-inflammatory properties. This compound has been shown to alleviate colitis in murine models by modulating inflammatory responses through inhibition of the NF-κB pathway and regulation of T helper cell balance. Additionally, Demethyleneberberine chloride acts as an AMPK activator, making it a valuable reagent for research into non-alcoholic fatty liver disease (NAFLD). -
HDAC Inhibitor
CM-444 is a potent inhibitor of histone deacetylases (HDACs) with an IC50 range of 6 nM to 0.6 μM, and demonstrates inhibition of DNA methyltransferases (DNMT) with IC50 values between 1.8 and 2.3 μM. This compound facilitates the differentiation of acute myeloid leukemia cells and exhibits significant anti-leukemic activity, enhancing survival rates in mouse models. CM-444 serves as a valuable tool for research into cancer epigenetics and the development of targeted therapies for leukemia. -
Proteasome Inhibitor
PR-39 is a natural proline- and arginine-rich antibacterial peptide that functions as a noncompetitive, reversible allosteric inhibitor of the proteasome. By binding to the α7 subunit of the proteasome, PR-39 effectively blocks the degradation of NF-κB inhibitor IκBα through the ubiquitin-proteasome pathway. This compound demonstrates key biological activities such as stimulating angiogenesis and inhibiting inflammatory responses, making it a valuable tool for research on myocardial infarction and inflammatory diseases. -
CTH/H2S/NF-κB/EMT Inhibitor
TKL002 is a selective inhibitor targeting the CTH/H2S/NF-κB/EMT signaling pathway, proven to penetrate the blood-brain barrier. It effectively induces G2/M phase cell cycle arrest and apoptosis in glioblastoma cells, simultaneously inhibiting their migration and invasion. This compound upregulates E-cadherin while downregulating N-cadherin and vimentin, making it a valuable tool for investigative studies in glioblastoma research. -
Survivin Inhibitor
MX107 is a selective survivin inhibitor known for its potent efficacy in suppressing the proliferation of triple-negative breast cancer (TNBC) cells. By inducing the degradation of survivin and inhibitor-of-apoptosis proteins (IAPs), MX107 effectively inhibits nuclear factor κB (NF-κB) activation in response to DNA damage. This compound enhances the tumoricidal effects of genotoxic treatments when used in conjunction with chemotherapeutic agents, making it a valuable tool in cancer research and therapy development. -
RIPK2 Inhibitor
CSLP43 is a selective inhibitor of RIPK2, demonstrating an IC50 of 19.9 nM against human RIPK2. By binding to the ATP-binding pocket of RIPK2, CSLP43 disrupts its interaction with the BIR2 domain of XIAP and cIAP1, effectively inhibiting RIPK2 ubiquitination and regulating NOD1- and NOD2-dependent inflammatory signaling pathways, as well as NF-κB activation. This compound is particularly relevant for research investigating Crohn's disease, Blau syndrome, early-onset sarcoidosis, and early-onset inflammatory bowel disease, due to its selectivity for the NOD1/NOD2 signaling pathway without affecting RIPK1 or RIPK3 activity. -
NF-κB Inhibitor/p53 Activator
CBLC100 is an NF-κB inhibitor and a p53 activator that exhibits potent anticancer properties. By targeting FACT, CBLC100 induces cytotoxicity through both p53-dependent apoptotic and non-apoptotic pathways. This compound is particularly relevant for research applications centered on cancers, including fibrosarcoma, making it a valuable tool for studying tumorigenesis and therapeutic responses. -
p53-MDM2 Inhibitor
p53-MDM2-IN-2 is an orally active inhibitor targeting the p53-MDM2 interaction, exhibiting a Ki value of 0.25 μM. This compound demonstrates antitumor activity through the inhibition of the NF-κB signaling pathway. It is valuable in research studies focusing on cancer therapy and elucidating the molecular mechanisms of tumor suppression. -
p53-MDM2 Inhibitor
p53-MDM2-IN-3 is a potent p53-MDM2 inhibitor with a Ki value of 0.25 μM, demonstrating oral bioavailability. This compound exhibits significant antitumor activity through its inhibition of the NF-κB signaling pathway. It serves as a valuable tool for cancer research, particularly in studies focused on targeting the p53-MDM2 interaction and the subsequent effects on tumor proliferation and survival. -
AURKC-IκBα Interaction Inhibitor
AKCI is an AURKC-IκBα interaction inhibitor with an IC50 value of 24.9 μM. It effectively induces G2/M cell cycle arrest in MDA-MB-231 cells by modulating the p53/p21/CDC2/cyclin B1 signaling pathway, while also inhibiting cell migration and invasion. Additionally, AKCI reduces colony formation and tumor growth, making it a valuable tool for investigating breast cancer mechanisms. -
Herbicide/Microtubule inhibitor
Ethalfluralin is a dinitroaniline herbicide that functions as a microtubule inhibitor. By disrupting intranuclear spindle formation, Ethalfluralin effectively obstructs nuclear division and cytokinesis in parasites. This compound also enhances phosphorylation of NF-κB and P38 MAPK while inhibiting the PI3K/AKT signaling pathway, leading to impaired mitochondrial functionality, apoptosis, endoplasmic reticulum stress, autophagy, and increased reactive oxygen species (ROS) production. Ethalfluralin is particularly relevant for research applications in toxoplasmosis and related parasitic diseases. -
NLRP3 Inhibitor
NLRP3-IN-78 is a potent inhibitor of the NLRP3 inflammasome, demonstrating a 46.72% inhibition rate in GSDMD-induced pyroptosis at a concentration of 5 μM. This compound effectively binds to the NLRP3 protein, hindering GSDMD-NT oligomerization and cleavage while also suppressing upstream NF-κB signaling. NLRP3-IN-78 serves as a valuable tool for investigating anti-inflammatory mechanisms and the role of NLRP3 in various disease models. -
FIKK9.1 Inhibitor
FIKK9.1-IN-1 is a selective inhibitor of the protein kinase FIKK9.1, targeting its ATP-binding residues. This compound demonstrates significant biological activity as an antimalarial agent, exhibiting an IC50 value of 2.68 μg/mL. By disrupting the life cycle of malaria parasites, FIKK9.1-IN-1 facilitates their elimination, making it a valuable tool for research focused on malaria intervention strategies. -
EPAC2 Inhibitor
MAY0132 is a potent and selective inhibitor of the EPAC2 pathway, exhibiting an IC50 of 0.4 μM. This compound significantly impedes the replication of human metapneumovirus (HMPV), adenovirus (AdV), and respiratory syncytial virus (RSV), while also decreasing cytokine and chemokine production induced by viral infections. Furthermore, MAY0132 inhibits NF-κB activation, underscoring its utility in research focused on antiviral mechanisms and respiratory virus pathogenesis. -
CDK8/19 Inhibitor
Senexin A hydrochloride is a selective inhibitor of cyclin-dependent kinases 8 and 19 (CDK8 and CDK19), with an IC50 of 280 nM for CDK8. It specifically targets and inhibits p21-induced transcription, while sparing other biological functions of p21. In addition, Senexin A hydrochloride effectively suppresses CMV-GFP induction and the p21 stimulatory activity of NF-κB-dependent promoters, making it a valuable tool for studying transcriptional regulation and cell signaling pathways. -
CDK8 Inhibitor
CDK8-IN-15 is a selective inhibitor of cyclin-dependent kinase 8 (CDK8), exhibiting a potent IC50 of 57 nM. This compound enhances the thermal stability of CDK8 while effectively inhibiting NF-κB signaling pathways. CDK8-IN-15 demonstrates promising biological activity in an in vitro psoriasis model induced by TNF-α, alleviating inflammation and promoting the expression of anti-inflammatory markers such as Foxp3 and IL-10. This makes it a valuable tool for research into psoriasis and related inflammatory disorders. -
ACAT Inhibitor
ACAT-IN-7 is an acyl-Coenzyme A:cholesterol acyltransferase (ACAT) inhibitor. This compound effectively inhibits ACAT activity, resulting in altered lipid metabolism and subsequent reduction in cholesterol esterification. ACAT-IN-7 is of particular interest in research exploring its potential role in inflammatory processes, as it inhibits NF-κB mediated transcription, which is crucial for various cellular responses. -
ACAT Inhibitor
ACAT-IN-2 is a selective inhibitor of acyl-Coenzyme A:cholesterol acyltransferase (ACAT). This compound effectively inhibits the NF-κB mediated transcriptional process, making it a valuable tool for research in cholesterol metabolism and inflammatory pathways. ACAT-IN-2 is primarily utilized in studies investigating dyslipidemia and its associated diseases, contributing to a deeper understanding of lipid regulation and associated pathophysiology. -
ACAT Inhibitor
ACAT-IN-10 is an acyl-Coenzyme A:cholesterol acyltransferase (ACAT) inhibitor that provides valuable insights into lipid metabolism. This compound is particularly useful in studying the regulation of cholesterol esters and their implications in various diseases, including atherosclerosis and metabolic disorders. Additionally, ACAT-IN-10 exhibits weak inhibition of NF-κB-mediated transcription, making it a potential tool for investigating inflammatory pathways. -
ACAT Inhibitor
ACAT-IN-4 hydrochloride is a selective acyl-Coenzyme A:cholesterol acyltransferase (ACAT) inhibitor. It disrupts cholesterol esterification, leading to a reduction in lipid accumulation in cells. This compound has significant implications for research in atherosclerosis, inflammation, and lipid metabolism, particularly through its ability to inhibit NF-κB mediated transcription. -
ACAT Inhibitor
ACAT-IN-9 is a selective acyl-Coenzyme A:cholesterol acyltransferase (ACAT) inhibitor that effectively disrupts the synthesis of cholesteryl esters. By inhibiting ACAT activity, ACAT-IN-9 also attenuates NF-κB mediated transcription, which plays a critical role in inflammation and immune responses. This compound is utilized in research focusing on lipid metabolism, cardiovascular diseases, and inflammation pathways. -
ACAT Inhibitor
ACAT-IN-4 is an acyl-Coenzyme A:cholesterol acyltransferase (ACAT) inhibitor that effectively impedes ACAT activity. This compound has been shown to inhibit NF-κB mediated transcription, making it a valuable tool for studying cholesterol metabolism and inflammatory responses. ACAT-IN-4 is suitable for research applications focusing on lipid regulation, atherosclerosis, and other related cardiovascular conditions. -
ACAT Inhibitor
ACAT-IN-10 dihydrochloride is an acyl-Coenzyme A:cholesterol acyltransferase (ACAT) inhibitor. This compound exhibits weak inhibition of NF-κB mediated transcription, highlighting its potential role in modulating inflammatory processes. It is primarily utilized in research focused on lipid metabolism and its implications in various diseases, including atherosclerosis and metabolic disorders. ACAT-IN-10 dihydrochloride serves as a valuable tool for investigating the biochemical pathways regulated by ACAT activity. -
ACAT Inhibitor
ACAT-IN-6 is a potent acyl-Coenzyme A:cholesterol acyltransferase (ACAT) inhibitor. This compound effectively inhibits NF-κB mediated transcription, making it a valuable tool for studying lipid metabolism and inflammatory pathways. ACAT-IN-6 is useful in research applications focused on cholesterol homeostasis and related diseases. -
ACAT Inhibitor
ACAT-IN-3 is an inhibitor of acyl-Coenzyme A:cholesterol acyltransferase (ACAT), targeting the cholesterol esterification pathway. This compound effectively inhibits NF-κB-mediated transcription, making it a valuable tool in studying pathways associated with inflammation and lipid metabolism. Its application in research may help elucidate the role of ACAT in various disease models, particularly those related to atherosclerosis and other metabolic disorders. -
ACAT Inhibitor
ACAT-IN-5 is a selective inhibitor of acyl-Coenzyme A:cholesterol acyltransferase (ACAT), a key enzyme involved in cholesterol metabolism. By inhibiting ACAT activity, ACAT-IN-5 has been shown to modulate NF-κB mediated transcription, thereby influencing inflammatory pathways and lipid metabolism. This reagent is vital for research applications exploring cholesterol homeostasis, atherosclerosis, and related metabolic disorders. -
HDAC Inhibitor
HDAC-IN-54 is a potent histone deacetylase (HDAC) inhibitor, exhibiting IC50 values of 25 nM for human HDAC1, 66 nM for HDAC2, 6.5 nM for HDAC3, and 281 nM for HDAC6. This compound effectively induces acetylation of α-tubulin and histone H3, promoting cancer cell apoptosis, particularly in synergy with cisplatin. HDAC-IN-54 is relevant for research applications in head and neck cancer, ovarian cancer, and tongue squamous cell carcinoma. -
MyD88 Inhibitor
T6167923 is a selective inhibitor of MyD88-dependent signaling pathways, targeting the Toll/IL-1 receptor (TIR) domain of MyD88 to disrupt its homodimeric formation. This compound effectively inhibits NF-κB-mediated Staphylococcus enterotoxin AP (SEAP) activity, demonstrating notable anti-inflammatory effects with IC50 values of 2.7 μM for IFN-γ, 2.9 μM for IL-1β, 2.66 μM for IL-6, and 2.66 μM for TNF-α. T6167923 serves as a valuable tool in studying the role of MyD88 signaling in inflammatory responses and therapeutic interventions. -
Myd88 Inhibitor
MyD88-IN-1 is a potent inhibitor of MyD88, targeting the interaction between TLR4 and MyD88. By suppressing the NF-κB signaling pathway, MyD88-IN-1 demonstrates significant biological activity relevant to cancer and inflammatory research. This compound serves as a valuable tool for elucidating the role of MyD88 in various disease processes and therapeutic interventions. -
Syk Inhibitor
DBMB is a selective inhibitor of spleen tyrosine kinase (Syk) that effectively attenuates Syk kinase activity. Its mechanism of action involves the suppression of NF-κB signaling, leading to a decrease in the production of key inflammatory mediators, including nitric oxide (NO) and prostaglandin E2 (PGE2). DBMB is suitable for investigations focused on inflammatory diseases and elucidating the role of Syk in immune response pathways. -
iNOS Inhibitor
Asperuloside is an iridoid compound derived from Hedyotis diffusa, primarily known for its role as an inducible nitric oxide synthase (iNOS) inhibitor. This compound exhibits notable anti-inflammatory properties by suppressing the NF-κB and MAPK signaling pathways. Asperuloside is valuable in studying inflammatory processes and developing therapeutic strategies for related diseases. -
NF-κB Inhibitor
Neocryptotanshinone is a potent NF-κB inhibitor derived from Salvia miltiorrhiza. This compound effectively suppresses lipopolysaccharide-induced inflammation by targeting and inhibiting the NF-κB and iNOS signaling pathways. It shows promise in research applications focused on inflammatory diseases and provides valuable insights into the mechanisms of immune response modulation. -
iNOS/Nf-Κb Inhibitor
Hymenoxin is a dual inhibitor of inducible nitric oxide synthase (iNOS) and nuclear factor kappa B (NF-κB), exhibiting IC50 values of 42.7 μM and 85.5 μM, respectively. This compound demonstrates the capacity to reduce oxidative stress by 16% at a concentration of 125 μg/mL. Hymenoxin is primarily utilized in research focused on inflammatory responses and related signaling pathways. Its inhibitory effects on key regulators make it valuable for studies investigating the roles of iNOS and NF-κB in various disease models. -
NOS Inhibitor
SDMA (p-hydroxyazobenzene-p′-sulfonate) is a potent endogenous inhibitor of nitric oxide synthase (NOS), making it a valuable tool for studying NOS-related pathways. This compound has been shown to activate NF-κB, leading to increased expression of pro-inflammatory cytokines such as IL-6 and TNF-α. Additionally, SDMA demonstrates stability in serum and plasma, allowing its use as a biomarker for assessing hepatic and renal dysfunction in various research applications. -
iNOS/ICAM-1 Inhibitor
Aloenin aglycone is an inhibitor of iNOS and ICAM-1, derived from aloe exudate. It effectively suppresses TNFα-induced NF-κB transcriptional activity with an IC50 of 18.7 μM. Additionally, at a concentration of 10 μM, it significantly reduces the expression of both inducible nitric oxide synthase (iNOS) and intercellular adhesion molecule 1 (ICAM-1) in HepG2 cells following TNFα stimulation. This compound serves as a valuable tool for investigating inflammatory pathways and potential therapeutic interventions in related conditions. -
FOXP3 Inhibitor
Peptide P60 is a potent FOXP3 inhibitor that disrupts the nuclear translocation of FOXP3, thereby decreasing its regulatory effects on NF-κB and NFAT signaling pathways. This action inhibits the immunosuppressive capabilities of regulatory T cells, facilitating the proliferation and activation of effector T cells. Experimental studies have shown that Peptide P60 can induce lymphoproliferative autoimmune syndrome in neonatal ICR mice and diminish the population of CD4+CD25+Foxp3+ T cells in the spleen. Additionally, it enhances the efficacy of peptide vaccines and recombinant adenovirus-based vaccines, making it valuable for research in tumor immunology, viral infections, and autoimmune conditions. -
RANKL Inhibitor
RANKL-IN-1 is a selective and orally bioactive inhibitor of Receptor Activator of Nuclear Factor-κB Ligand (RANKL), displaying a KD value of 7.6 μM. This compound effectively inhibits osteoclastogenesis with an IC50 of 0.07 μM and a selectivity index of 82.57. RANKL-IN-1 directly interacts with RANKL, preventing downstream activation of the NF-κB and MAPK signaling pathways. It is a valuable tool for investigating metabolic disorders, particularly osteoporosis. -
STING Inhibitor
STING-IN-4 is a potent STING inhibitor that effectively reduces the expression and activation of STING and nuclear factor-κB (NF-κB) signaling pathways. This compound exhibits significant anti-inflammatory activity, making it a valuable tool for investigating sepsis and related inflammatory conditions. Researchers can utilize STING-IN-4 to explore the therapeutic potential of modulating STING activity in various biological contexts. -
NF-κB Inhibitor
Eupenicisirenin C is a potent inhibitor of the NF-κB signaling pathway. This compound effectively suppresses the cGAS-STING pathway, demonstrating significant potential in modulating inflammatory responses. Notably, Eupenicisirenin C inhibits RANKL-induced osteoclast differentiation in bone marrow macrophages, making it a valuable tool for research into bone metabolism and inflammatory diseases. -
BACH1 Inhibitor
ASP-8731 is a potent BACH1 inhibitor that enhances NRF2-mediated gene transcription, thereby activating antioxidant and anti-inflammatory pathways. This compound significantly upregulates the expression of key genes such as HMOX1 and FTH1, and increases fetal hemoglobin (HbF) levels, promoting F-cell production in hydroxyurea-unresponsive cells. Additionally, ASP-8731 mitigates inflammatory responses by downregulating VCAM1, ICAM-1, and NF-κB (p65) phosphorylation. Its ability to relieve glutathione depletion and microcirculatory stasis suggests potential applications in the treatment of sickle cell disease and other hematological disorders. -
COX-2 Inhibitor
COX-2-IN-51 is a selective COX-2 inhibitor exhibiting an IC50 of 70.7 nM. It effectively reduces LPS-induced release of nitric oxide (NO) and prostaglandin E2 (PGE2), as well as the expression of COX-2 and inducible nitric oxide synthase (iNOS), and inhibits the NF-κB signaling pathway. This compound demonstrates anti-inflammatory and analgesic properties in various murine models by targeting the NF-κB cascade, while presenting a lower risk of gastrointestinal side effects compared to traditional nonsteroidal anti-inflammatory drugs. -
COX-2/15-LOX Inhibitor
COX-2/15-LOX-IN-5 is a potent dual inhibitor of cyclooxygenase-2 (COX-2) and 15-lipoxygenase (15-LOX). This compound effectively attenuates lipopolysaccharide-induced NF-κB activation in RAW 264.7 macrophages, highlighting its role in modulating inflammatory responses. COX-2/15-LOX-IN-5 exhibits significant anti-inflammatory and antioxidant properties, making it a valuable tool for research into inflammatory diseases and other related biological processes. -
COX-2/TAK1-NF-κB Inhibitor
BPD is a selective inhibitor of COX-2 and TAK1-NF-κB, exhibiting an IC50 of 18.5 μM for COX-2. This compound effectively reduces the transcriptional expression of key pro-inflammatory cytokines, including iNOS, TNF-α, IL-6, and IL-1β, thereby demonstrating notable anti-inflammatory properties. BPD has been shown to inhibit carrageenan-induced paw edema and mitigate LPS-induced septic mortality, making it a valuable tool for research in inflammation and related pathways. -
NF-κB/COX Inhibitor
Methoxycoronarin D is a potent inhibitor of NF-κB, demonstrating an IC50 value of 7.3 μM. Additionally, it selectively inhibits cyclooxygenase-1 (COX-1), with an IC50 value of 0.9 μM. This compound is relevant for research applications focused on inflammation and cancer due to its ability to modulate critical signaling pathways. -
COX-2 Inhibitor
Cavidine is a selective COX-2 inhibitor that exhibits potent anti-inflammatory properties. It is particularly useful in research concerning skin injuries, hepatitis, cholecystitis, and scabies. Additionally, Cavidine has been shown to alleviate LPS-induced acute lung injury through modulation of the NF-κB signaling pathway, making it a valuable compound for studying inflammation-related conditions. -
Sphingomyelinase Inhibitor, K-Ras Inhibitor, H-Ras Inhibitor, NF-κB Inhibitor
Avicin G is a potent inhibitor of sphingomyelinases, specifically targeting neutral sphingomyelinases (SMPD2/3) and acid sphingomyelinase (SMPD1). This compound elevates intracellular sphingomyelin levels and modulates the distribution of sphingomyelin, disrupting signal transduction pathways in oncogenic K-Ras and H-Ras. Avicin G exhibits significant biological activity, including the reduction of ERK and Akt phosphorylation and alterations in lysosomal pH. Its applications extend to research on pancreatic ductal adenocarcinoma and non-small cell lung cancer. -
AP-1/NF-κB Activation Inhibitor
SPC 839 is an orally active inhibitor that targets AP-1 and NF-κB mediated transcriptional activation, demonstrating an IC50 of 0.008 μM. This compound is essential for studying pathways associated with inflammation, cancer progression, and cellular stress responses. Its potent inhibition of key transcription factors makes it a valuable tool for researchers investigating the role of AP-1 and NF-κB in various biological processes. -
NF-κB Inhibitor
Ganoderic acid H is a lanostane-type triterpene that functions as an NF-κB inhibitor. It effectively suppresses the growth and invasive behavior of breast cancer cells by inhibiting the activity of transcription factors AP-1 and NF-κB. This compound holds potential for research applications in cancer biology, particularly for studies focusing on the modulation of signaling pathways involved in tumor progression and metastasis.
