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BRD 4/p38α/BRDT Inhibitor
SB-284851-BT is a selective inhibitor of BRD4, p38α, and BRDT. It effectively inhibits BRD4-BD1 with an IC50 of 1.7 µM, p38α with a Kd of 0.47 nM, and exhibits additional inhibitory activity against BRDT and BRD4 with IC50 values of 18 µM and 3.7 µM, respectively. SB-284851-BT significantly reduces IL-8 production through p38α inhibition and downregulates crucial oncogenic pathways such as c-Myc and NF-κB via BRD4 inhibition. This compound has potential applications in cancer research and therapeutic development targeting cellular signaling pathways. -
BRD4 BD1 Inhibitor
ZL0516 is a selective inhibitor of the BRD4 bromodomain 1 (BD1), demonstrating potent activity in modulating epigenetic regulation. It effectively suppresses inflammatory bowel disease (IBD) through inhibition of the BRD4/NF-κB signaling pathway, which plays a critical role in inflammation and immune responses. This compound is primarily utilized in research focusing on the development of therapeutic strategies for IBD and related inflammatory conditions. -
Inflammatory Pathway Inhibitor, Oxidative Stress Inhibitor, Cancer Pathway Inhibitor
Matairesinol is an orally active bioactive compound that functions as an inflammatory pathway, oxidative stress, and cancer pathway inhibitor. It effectively inhibits the phosphorylation of MAPK, JNK, and NF-κB, while downregulating RANKL-induced NFATc1 expression and activity, and suppressing the activation of the PI3K/AKT/FOXO1 pathway. Matairesinol is applicable in research on sepsis-mediated brain injury, osteoporosis, heart failure, atopic dermatitis, and various cancer models. -
JNK Inhibitor
Salicortin is a phenolic glycoside that functions as a JNK inhibitor. It effectively inhibits osteoclast differentiation and bone resorption by down-regulating the JNK and NF-κB/NFATc1 signaling pathways. Salicortin exhibits a range of biological activities, including anti-amnesic, anti-adipogenic, and immune-modulatory effects, making it a valuable tool for research in bone metabolism, neurobiology, and immunology. -
NF-κB Inhibitor
Esculentoside H (EsH) is a saponin with inhibitory effects on the NF-κB signaling pathway. It exhibits notable anti-tumor activity, primarily through the modulation of TNF release. EsH has been shown to suppress colon cancer cell migration by inhibiting JNK1/2 and reducing the expression of matrix metalloproteinases-9 (MMP-9), making it a valuable tool for research in cancer biology and therapeutic interventions. -
NF-κB/AP-1 Inhibitor
IQ-1S is an inhibitor of NF-κB and activating protein 1 (AP-1), exhibiting an IC50 of 1.8 μM. It demonstrates significant binding affinity for all three JNK isoforms, with Kd values of 87 nM for JNK3, 360 nM for JNK2, and 390 nM for JNK1. IQ-1S is valuable for researchers investigating the role of JNK signaling pathways and their implications in inflammation and cancer. -
JNK2 Inhibitor
JNK2-IN-1 is a selective inhibitor of JNK2, displaying a dissociation constant (Kd) of 79.2 μM. This compound exhibits anti-inflammatory properties by reducing the secretion of pro-inflammatory cytokines TNF-α and IL-6 through the inhibition of the NF-κB/MAPK signaling pathway. JNK2-IN-1 has demonstrated therapeutic potential in alleviating symptoms associated with LPS-induced acute lung injury (ALI) and sepsis, making it valuable for research in inflammation and related diseases. -
NF-κB p65 Inhibitor, p38 MAPK Inhibitor
PSMα3 is an inhibitor of NF-κB p65 and p38 MAPK, playing a significant role in modulating inflammatory pathways. This compound forms membrane pores and interacts with the human insulin B chain, inhibiting insulin aggregation and contributing to cytotoxic effects through α-type amyloid-like fibril formation. PSMα3 is valuable for research on spondyloarthritis, rheumatoid arthritis, insulin-derived amyloidosis, and infections caused by Staphylococcus aureus. -
NF-κB/MAPK Inhibitor
NF-κB/MAPK-IN-1 is a potent inhibitor of the NF-κB and MAPK signaling pathways, exhibiting significant biological activity in the modulation of inflammatory responses. It effectively reduces nitric oxide (NO) production with an IC50 of 6.96 µM and inhibits the activation of iNOS, COX-2, ERK, and p38 signaling pathways induced by LPS. This compound is valuable for research applications focused on inflammatory diseases, including rheumatoid arthritis. -
NF-κB/MMP9/MAPK Inhibitor
Isoliquiritin apioside is an inhibitor of NF-κB, MMP9, and MAPK signaling pathways. It has been shown to significantly reduce PMA-induced MMP9 activity and suppress the activation of MAPK and NF-κB. This compound is relevant for research applications focused on cancer biology, particularly in the investigation of mechanisms underlying cell invasiveness and angiogenesis in both cancer and endothelial cells. -
IRAK4 Inhibitor
UR241-2 is a selective inhibitor of IRAK4, targeting the IL-1–induced IRAK1/4 signaling pathway. It effectively suppresses NF-κB activation and the phosphorylation of p65 and p38, contributing to a reduction in leukemia stem cell clonogenicity. UR241-2 also serves as a valuable ligand for developing PROTAC degraders targeting IRAK4, making it a suitable tool for research in acute myeloid leukemia. -
TRPA1 Inhibitor
Aurothiomalate disodium acts as a TRPA1 inhibitor, effectively blocking NF-κB activation and inhibiting iNOS expression. This compound fosters the M2 transformation of macrophages and enhances the expression of TREM-2 and arginase-1. Aurothiomalate disodium is applicable in research concerning liver fibrosis, cirrhosis, and arthritis, providing insights into inflammation and tissue repair mechanisms. -
LUBAC Inhibitor
HOIPIN-8 is a highly potent inhibitor of the linear ubiquitin chain assembly complex (LUBAC), exhibiting an IC50 value of 11 nM. As a derivative of HOIPIN-1, it offers significantly enhanced inhibition, demonstrating a 255-fold increase in potency for petit-LUBAC, along with 10-fold and 4-fold increases in inhibiting LUBAC and TNF-α-mediated NF-κB activation, respectively. HOIPIN-8 serves as an essential research tool for investigating the cellular functions of LUBAC and its role in various biological processes. -
Na+/K+-ATPase Inhibitor
(-)-γ-Cuparenol is a sesquiterpene compound that acts as an inhibitor of Na+/K+-ATPase, with an IC50 value of 23.6 μg/mL in porcine models. It has demonstrated the ability to reduce phytohemagglutinin (PHA)-induced activation of NF-AT and NF-κB in Jurkat cells, indicating potential applications in immunoregulation. Additionally, (-)-γ-Cuparenol exhibits antibacterial activity against certain Gram-positive and some Gram-negative bacteria, as well as weak inhibitory effects on Candida albicans. This compound is relevant for research exploring cardiovascular diseases and bacterial infections. -
Bacterial Inhibitor/Anti-inflammatory Agent
Cyclo(L-Pro-L-Val) is a peptide-based compound that functions as a bacterial inhibitor and anti-inflammatory agent. It exhibits antimicrobial activity against plant pathogens, such as R. fascians, and demonstrates significant inhibition of critical signaling molecules like IKKα, IKKβ, NF-κB, iNOS, and COX-2, contributing to its anti-inflammatory properties. This compound is valuable for research applications in developing biopesticides and investigating inflammation-related diseases. -
TrxR1 Inhibitor
Evernic Acid is a potent inhibitor of thioredoxin reductase 1 (TrxR1), demonstrating significant antiproliferative effects on human breast cancer cells. It disrupts the NF-κB signaling pathway by preventing p65 nuclear translocation and IκBα phosphorylation, which subsequently reduces inflammatory mediators. In addition to its role as an antioxidant and neuroprotective agent, Evernic Acid protects neurons from oxidative stress and mitochondrial dysfunction. Furthermore, it inhibits key enoyl reductases in Plasmodium falciparum and downregulates quorum sensing and biofilm formation in Pseudomonas aeruginosa, showcasing its antibacterial and antifungal properties. This compound is valuable for research focused on breast cancer, neurodegenerative diseases, and microbial infections. -
PKC Inhibitor
PKC-IN-4 is a selective inhibitor of atypical protein kinase C (aPKC) with an IC50 of 0.52 µM. This compound effectively inhibits TNF-α-induced NF-κB signaling in vitro, making it a valuable tool for studies involving inflammatory responses. Additionally, PKC-IN-4 has been shown to block VEGF- and TNF-α-induced permeability across the retinal vasculature, highlighting its potential in retinal disease research and vascular permeability exploration. -
Survivin Inhibitor
Isonanangenine B is a selective inhibitor of survivin, exhibiting an IC50 of 1.6 µM. It effectively obstructs the interaction of critical transcription factors, including Stat3 and NF-κB, with the survivin promoter. This compound holds potential for advancing cancer research, particularly in elucidating the mechanisms of survivin modulation in tumorigenesis. -
TNF-α/NF-κB Inhibitor
TNF-α-IN-28 is a selective inhibitor of TNF-α and NF-κB, demonstrating significant anti-inflammatory activity. This compound effectively inhibits the expression of both TNF-α and NF-κB by targeting the TNF-α dimer. TNF-α-IN-28 is intended for use in research applications focused on inflammation, immune response modulation, and related signaling pathways. -
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. -
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. -
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. -
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. -
Influenza Virus Inhibitor
Amizon is an orally effective antiviral agent targeting the influenza virus. It inhibits viral replication and restricts RNA synthesis, while simultaneously reducing the mRNA expression of pro-inflammatory mediators such as COX-1, COX-2, NF-κB, TGF-β1, IL-1, and IL-6. Additionally, Amizon enhances the secretion and mRNA expression of the anti-inflammatory cytokine IL-10 and exhibits antioxidant properties, inhibiting the oxidative activity of macrophages. This compound is of interest in research focused on influenza and acute respiratory viral infections. -
Parasite Inhibitor
8-Deoxygartanin, a prenylated xanthone derived from Garcinia mangostana, serves as a selective inhibitor of butyrylcholinesterase (BChE). This compound demonstrates significant antiplasmodial activity, with an IC50 value of 11.8 μM against the W2 strain of Plasmodium falciparum. Additionally, 8-Deoxygartanin inhibits NF-κB (p65) activation, displaying an IC50 of 11.3 μM, making it a valuable reagent for research in parasitic infections and inflammation pathways. -
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. -
cGAS Inhibitor
cGAS-IN-9 is an inhibitor of cyclic guanosine monophosphate-adenosine monophosphate synthase (cGAS) with IC50 values of 27.5 nM and 5.15 μM for human and murine cGAS, respectively. This compound demonstrates weak inhibitory activity against human soluble adenylate cyclase, with an IC50 of 26.4 μM. cGAS-IN-9 significantly reduces dsDNA-induced expression of IFNB1 and CXCL10, as well as inhibits the activation of the NF-κB pathway in human immune cells. It is a valuable tool for research on cGAS-dependent inflammatory diseases. -
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). -
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. -
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. -
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.

