NF-κB Activator

Urocortin II, human is a selective endogenous peptide agonist of type-2 corticotropin-releasing factor (CRF2) receptor. Urocortin II, human has an effect of promoting satiet and neuroprotective effect. Urocortin II, human also has bactericidal, antiparasitic and pro-inflammation activity. Urocortin II, human can activate NF-κB pathway and ERK1/2 MAP kinase. Urocortin II, human can reduce pulmonary arterial hypertension and shows cardiac protection effect. Urocortin II, human can be used for the researches of infection, inflammation, metabolic, neurological and cardiovascular disease.

NF-κΒ activator 2 is a potent and orally active NF- B activator, with an EC₅₀ of 1.58 μM. NF-κΒ activator 2 induces SOD₂ through increasing NF- B expression and activation. NF-κΒ activator 2 can be used for the research of amyotrophic lateral sclerosis (ALS).

Pam2CSK4 TFA is a TLR2 agonist. Pam2CSK4 TFA induces the expression of iNOS and NO in macrophage cell lines via TBK1 and MyD88 molecules. Pam2CSK4 TFA activates the NF-κB and Bruton's tyrosine kinase signaling pathways in platelets, and promotes platelet-endothelial cell interactions. TLR2 activation triggered by Pam2CSK4 TFA expands myeloid-derived suppressor cells (MDSCs) and suppresses anti-tumor immune responses in the tumor microenvironment. Pam2CSK4 TFA acts as a Th2-polarizing adjuvant in mouse vaccine models against Leishmania major and Brugia malayi. Pam2CSK4 TFA can be used in the research of various diseases, including thromboinflammatory diseases, sepsis, atherosclerosis, heart failure, influenza, lymphoma, melanoma, cutaneous leishmaniasis and lymphatic filariasis.

Hydroxycitric acid is an orally active, multi-target, multi-bioactive organic acid. activates Nrf2 and its downstream molecule GPX4, increases glutathione levels, and thereby inhibits ferroptosis. Hydroxycitric acid activates the Nrf2/Keap1 and ACLY/NF-κB signaling pathways, upregulates the activities of antioxidant enzymes such as superoxide dismutase, reduces MDA content, thereby alleviating oxidative stress and renal tubular epithelial cell apoptosis, and improves pulmonary vascular and right ventricular remodeling. Hydroxycitric acid activates both the AMPK and mTORC1/S6K pathways, triggers the unfolded protein response, arrests the cancer cell cycle, and induces DNA fragmentation.

2-Oleoylglycerol (2-OG) is a lipid found in the diet. It is a GPR119 agonist, with an EC₅₀ value of 2.5 μM in activating hGPR119 in transiently transfected COS-7 cells. 2-Oleoylglycerol enhances the inflammatory response of macrophages and promotes fibrosis by activating the GPR119/TAK1/NF-κB/TGF-β1 signaling pathway. It also stimulates glucagon-like peptide 1 (GLP-1) secretion in vivo. 2-Oleoylglycerol is expected to be used in the research of non-alcoholic steatohepatitis (NASH) .

Fluopyram is an orally active succinate dehydrogenase inhibitor, antifungal and nematicide. Fluopyram inhibits succinate dehydrogenase activity, activates CAR/PXR nuclear receptors, and increases caspase-3, TNF-α and NF-κB. Fluopyram inhibits the growth of F. virguliforme, Botrytis cinerea and Alternaria solani with EC₅₀ values of 3.35, 5.389 and 0.244 µg/mL, respectively. Fluopyram induces liver and thyroid tumor formation. Fluopyram is nephrotoxic and embryotoxic.

Protegrin-1 is an orally active antibacterial peptide. Protegrin-1 activates ERK, COX2, NFκB, inhibits Apoptosis, and NO production. Protegrin-1 has antibacterial activity against S. aureus, E. faecium, E. coli, P. aeruginosa and K. Pneumoniae, with MBC values between 10 and 20 µM. Protegrin-1 has antiviral activity against dengue NS2B-NS3. Protegrin-1 has anti-inflammatory activity. Protegrin-1 is used in the study of inflammatory diseases and infections.

RS 09 TFA is an LPS (HY-D1056) peptide mimic and TLR4 agonist. RS 09 TFA can bind to TLR-4 and activate NF-κB. RS 09 TFA can function as an adjuvant in vivo, enhancing the antigen-specific immune response.

Gypenoside L is a saponin that can be found in Gynostemma pentaphyllum. Gypenoside L increases the SA-β-galactosidase activity, promotes the production of senescence-associated secretory cytokines. Gypenoside L also can activate p38 and ERK MAPK pathways and NF-κB pathway to induce senescence. Gypenoside L exhibits anti-tumor and anti-inflammatory activities.

Nε-(Carboxymethyl)-L-lysine (CML) is an orally active advanced glycation end product. Nε-(Carboxymethyl)-L-lysine upregulates the expression of PLK1 and CEP20, and induces the activation of RAGE and ERK/NFκB. Nε-(Carboxymethyl)-L-lysine drives centrosome amplification. Nε-(Carboxymethyl)-L-lysine induces malignant transformation of hepatocytes and promotes the development of hepatocellular carcinoma. Nε-(Carboxymethyl)-L-lysine induces epithelial-mesenchymal transition in osteosarcoma cells and enhances their migration and invasion properties.

Triphenyl phosphate is an orally active, blood-brain barrier-permeable aryl organophosphate flame retardant and endocrine disruptor. Triphenyl phosphate disrupts mitochondrial dynamic balance through oxidative stress, induces excessive mitophagy and apoptosis, and ultimately leads to myocardial fibrosis. In the brain, Triphenyl phosphate activates the NF-κB inflammatory pathway by disrupting the gut microbiota, alters tryptophan metabolism and elevates neurotoxins, thereby inducing anxiety- and depression-like behaviors. In the skeletal and reproductive systems, Triphenyl phosphate inhibits osteoblast differentiation and induces germ cell apoptosis by suppressing the MAPK/ERK pathway and activating the JNK signal, respectively. In adipose and placental tissues, Triphenyl phosphate promotes lipid accumulation by activating the PI3K/AKT-PPARγ axis, and disrupts placental metabolism via the MAOA/ROS/NF-κB cascade, impairing neurodevelopment of offspring.

CHPG is a selective mGluR5 agonist, and attenuates SO₂-induced oxidative stress and inflammation through TSG-6/NF-κB pathway in BV2 microglial cells. CHPG protects against traumatic brain injury (TBI) in vitro and in vivo by activation of the ERK and Akt signaling pathways.

Melamine is an orally active inducer of Apoptosis. Melamine induces animal disease models. Melamine affects the activity of Sertoli cell and can be used for research on male reproductive function. Melamine also has neurotoxicity and nephrotoxicity. Melamine induces cognitive impairment and acute kidney injury models. Melamine can also be used to induce bladder cancer and urinary stone models.

ADP-β-S (Adenosine 5'-(β-thiodiphosphate)) trilithium is a non-hydrolyzable ADP analog and a P2Y12 receptor agonist. ADP-β-S trilithium activates the P2Y12 receptor in microglia, thereby triggering downstream inflammatory signaling pathways. ADP-β-S trilithium activates P2Y purinergic receptors in rat pancreatic β cells and enhances glucose-induced insulin secretion. ADP-β-S trilithium can be used in the research of diseases such as inflammation and diabetes.

TriDAP dihydrochloride (L-Ala-γ-D-Glu-meso-diaminopimelic acid dihydrochloride) is a NOD1 agonist with a K_d value of 34.5 μM. TriDAP dihydrochloride enhances the binding of NOD1-RICK, promotes RICK phosphorylation, and activates the NF-κB, TAK1, MEK/ERK, p38 and interferon response pathways. TriDAP dihydrochloride downregulates Runx2 via increasing ubiquitination and reduces trabecular bone parameters. TriDAP dihydrochloride decreases IκBα levels and increases p65 levels. TriDAP dihydrochloride induces the secretion of proinflammatory mediators IL-8 and prostaglandins, triggers tissue inflammation and innate immune activation, and inhibits SARS-CoV-2 replication in lung epithelial cells. TriDAP dihydrochloride increases the RANKL/OPG ratio in mice, reduces bone mass and enhances osteoclast activity, and inhibits new bone formation by decreasing the mineralization deposition rate in mice. TriDAP dihydrochloride can be used in research related to pulpitis, chronic ulcerative colitis, Crohn's disease and SARS-CoV-2 infection.

Arundic Acid is an orally effective astrocyte function modulator and neuroprotective agent. Arundic Acid increases the expression and function of the astrocytic glutamate transporter EAAT1 by activating the ERK, Akt and NF-κB pathways. Arundic Acid attenuates retinal ganglion cell death in a normal-tension glaucoma model. Arundic Acid exerts neuroprotective effects in a mouse model of Parkinson's disease. Arundic Acid is a S100β protein synthesis inhibitor that prevents neurological deficits and brain tissue damage after intracerebral hemorrhage in rats. Arundic Acid downregulates neuroinflammation and astrocytic dysfunction after status epilepticus in immature rats. Arundic Acid is applicable to research related to Parkinson's disease, cerebral ischemia, glaucoma, intracerebral hemorrhage and epilepsy.

CHPG sodium salt is a selective mGluR5 agonist, and attenuates SO₂-induced oxidative stress and inflammation through TSG-6/NF-κB pathway in BV2 microglial cells. CHPG sodium salt protects against traumatic brain injury (TBI) in vitro and in vivo by activation of the ERK and Akt signaling pathways..

Phorbol 12-myristate 13-acetate (PMA; TPA; Phorbol myristate acetate) (Standard) is the analytical standard of Phorbol 12-myristate 13-acetate. This product is intended for research and analytical applications.

Estragole (4-Allylanisole) is a relatively nontoxic volatile terpenoid ether and major component of the essential oil from many plants. Estragole significantly triggers Apoptosis, suppresses LPS-induced intracellular ROS production. Estragole activats Nrf-2 and regulates NF-κB. Estragole has anti-toxoplasma, anti-inflammatory, anti-edema, antioxidant and immunomodulatory properties. Estragole blocks DRG neuron excitability. Estragole has improves gastric ulcer activity.

DpC is a selective, orally active iron chelator with anticancer activity. DpC acts on signaling pathway-related targets such as JNK, NF-κB, and its activity is competitively inhibited by another iron chelator Dp44mT (HY-18973). By chelating intracellular iron and copper ions in tumor cells to form redox-active complexes, DpC induces oxidative stress, activates the JNK, NF-κB pathways and downregulates IκBα, upregulates the expressions of neuroglobin and cytoglobin, activates caspase 3/9 to induce tumor cell apoptosis. It also overcomes P-glycoprotein-mediated multidrug resistance through a lysosome-targeting mechanism, and exhibits broad-spectrum synergistic effects when combined with various chemotherapeutic agents. DpC inhibits tumor metastasis and increases TNF-α levels in the tumor microenvironment to enhance endogenous immune responses. DpC is applicable to the research of various malignancies including neuroblastoma, pancreatic cancer, prostate cancer, lung cancer, and breast cancer.