COX-2/5-LOX-IN-1 (compound 3a) is a potent and dual inhibitor of COX-2/5-LOX. COX-2/5-LOX-IN-1 is a benzothiophen-2-yl pyrazole carboxylic acid derivative. COX-2/5-LOX-IN-1 shows the most potent analgesic and anti-inflammatory activities surpassing that of Celecoxib and Indomethacin. COX-2/5-LOX-IN-1 shows potent COX-1, COX-2 and 5-LOX inhibitory activity with IC50s of 12.13, 0.4 and 4.96 μM, respectively[1].
Ketoprofen (RP-19583) lysinate is a non-steroidal anti-inflammatory agent. Ketoprofen lysinate can inhibit the activity of cyclooxygenase with IC50 values of 2 nM (COX-1) and 26 nM (COX-2). which is potential in the research of inflammation, immunology, and metabolic disease such as obesity[1][2][3].
Esculentoside A (EsA), a kind of triterpene saponin isolated from roots of Phytolacca esculenta[1].Esculentoside A (EsA) possesses anti-inflammatory activity in acute and chronic experimental models[2], has selective inhibitory activity towards cyclooxygenase-2 (COX-2)[1].Esculentoside A (EsA) suppresses inflammatory responses in LPS-induced acute lung injury (ALI) through inhibition of the nuclear factor kappa B (NF-ΚB) and mitogen activated protein kinase (MAPK) signaling pathways[3].
Ethyl Caffeate is a natural phenolic compound isolated from Bidens pilosa. Ethyl caffeate suppresses NF-κB activation and its downstream inflammatory mediators, inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and prostaglandin E2 (PGE2) in vitro or in mouse skin[1].
Veratric acid-d6 is deuterium labeled Veratric acid. Veratric acid (3,4-Dimethoxybenzoic acid) is an orally active phenolic compound derived from vegetables and fruits, has antioxidant[1] and anti-inflammatory activities[3]. Veratric acid also acts as a protective agent against hypertension-associated cardiovascular remodelling[2]. Veratric acid reduces upregulated COX-2 expression, and levels of PGE2, IL-6 after UVB irradiation[3].
Ginsenoside Rg3 is the main component of Red ginseng. Ginsenoside Rg3 inhibits Na+ and hKv1.4 channel with IC50s of 32.2±4.5 and 32.6±2.2 μM, respectively. Ginsenoside Rg3 also inhibits Aβ levels, NF-κB activity, and COX-2 expression.
Ibuprofen D3 is a deuterium labeled Ibuprofen. Ibuprofen is a COX-1 and COX-2 inhibitor with IC50s of 13 μM and 370 μM[1].
Byakangelicol, isolated from Angelica dahurica, inhibits interleukin-1beta (IL-1beta) -induced prostaglandin E2 (PGE2) release in A549 cells mediated by suppression of cyclooxygenase-2 (COX-2) expression and the activity of COX-2 enzyme. Byakangelicol has therapeutic potential as an anti-inflammatory drug on airway inflammation[1].
COX-2-IN-22 (Compound 4h) is a COX-2 inhibitor with an IC50 of 8.6 µM. COX-2-IN-22 also inhibits AChE, BChE, β-Secretase, LOX-5 and DPPH with IC50 values of 2.8, 6.3, 15.3, 13.9 and 6.8 µM, respectively. COX-2-IN-22 can cross BBB[1].
Ibuprofen-13C,d3 is the 13C- and deuterium labeled. Ibuprofen is an anti-inflammatory agent targeting COX-1 and COX-2 with IC50s of 13 μM and 370 μM, respectively.
Ibuprofen ((±)-Ibuprofen) L-lysine is a potent orally active, selective COX-1 inhibitor with an IC50 value of 13 μM. Ibuprofen L-lysine inhibits cell proliferation, angiogenesis, and induces cell apoptosis. Ibuprofen L-lysine is a nonsteroidal anti-inflammatory agent and a nitric oxide (NO) donor. Ibuprofen L-lysine can be used in the research of pain, swelling, inflammation, infection, immunology, cancers[1][2][3][4][5][6][7][8].
Shizukaol B is a lindenane-type dimeric sesquiterpene, used to be isolated from the whole plant of Chloranthus henryi. Shizukaol B has anti-inflammatory effect against lipopolysaccharide (LPS)-induced activation of BV2 microglial cells. Shizukaol B inhibits iNOS and COX-2, and suppresses NO production, TNF-α, and IL-1β expression[1].
Nimesulide D5 is a deuterium labeled Nimesulide. Nimesulide is a selective COX-2 inhibitor, with IC50s of 70 nM-70 μM in a time-dependent manner, but it shows no effect on COX-1 (IC50 >100 μM). Nimesulide has potent anti-inflammatory, analgesic and antipyretic properties[1][2].
AL-8417 is an enzyme inhibitor. It acting as an antioxidant, anti-inflammatory, and cytostatic agent. It also has the ability to suppress vitrectomy-induced posterior lens fiber changes.
Moracin C, a natural product, is an anti-inflammatory agent. Moracin C inhibits LPS-activated reactive oxygen species (ROS) and nitric oxide (NO) release from cells[1].
Nitroaspirin (NCX 4016) is a nitric oxide (NO) donor and a nitro-derivative of Aspirin, which combines with Nitroaspirin to inhibit cyclooxygenase. Nitroaspirin (NCX 4016) has antithrombotic and anti-platelet properties and acts as a direct and irreversible inhibitor of COX-1. Nitroaspirin (NCX 4016) causes significant induction of cell cycle arrest and apoptosis in Cisplatin-resistant human ovarian cancer cells via down-regulation of EGFR/PI3K/STAT3 signaling and modulation of Bcl-2 family proteins[1][2][3][4].
Taraxerol acetate is a COX-1 and COX-2 inhibitor with IC50 values of 116.3 μM and 94.7 μM, respectively. Taraxerol acetate the has the anticancer potential and induces cell apoptosis[1].
Indomethacin heptyl ester is a selective COX-2 inhibitor with IC50 of 0.04 μM, exhibits anti-inflammatory activity[1].
Eltenac, a non-steroidal anti-inflammatory drug (NSAID), is a COX inhibitor. Eltenac shows IC50 of 0.03 μM for both COX-1 and COX-2 in isolated human whole blood[1].
Aspirin (Acetylsalicylic Acid) lithium is an orally active, potent and irreversible inhibitor of cyclooxygenase COX-1 and COX-2, with IC50 values of 5 and 210 μg/mL, respectively. Aspirin lithium induces apoptosis. Aspirin lithium inhibits the activation of NF-κB. Aspirin lithium also inhibits platelet prostaglandin synthetase, and can prevent coronary artery and cerebrovascular thrombosis[1][2][3][4][5][6].
Coenzyme Q0 (CoQ0) is a potent, oral active ubiquinone compound can be derived from Antrodia cinnamomea. Coenzyme Q0 induces apoptosis and autophagy, suppresses of HER-2/AKT/mTOR signaling to potentiate the apoptosis and autophagy mechanisms. Coenzyme Q0 regulates NFκB/AP-1 activation and enhances Nrf2 stabilization in attenuation of inflammation and redox imbalance. Coenzyme Q0 has anti-angiogenic activity through downregulation of MMP-9/NF-κB and upregulation of HO-1 signaling[1][2][3].
Triflusal-d3 is deuterium labeled Triflusal.
Desmethyl Celecoxib (compound 3b) is a selective cyclooxygenase-2 (COX-2) inhibitor (IC50=32 nM) with anti-inflammatory activities. Desmethyl Celecoxib is an analog of Celecoxib and with the optimal yield of 75%[1].
Salicylic acid inhibits cyclo-oxygenase-2 (COX-2) activity independently of transcription factor (NF-κB) activation.
Indomethacin (Indometacin) sodium is a potent, orally active COX1/2 inhibitor with IC50 values of 18 nM and 26 nM for COX-1 and COX-2, respectively. Indomethacin sodium has anticancer activity and anti-infective activity. Indomethacin sodium can be used for cancer, inflammation and viral infection research.[1][2][3].
Dexketoprofen trometamol (Dexketoprofen tromethamine salt) is an orally active non-selective COX inhibitor. Dexketoprofen trometamol has a pain-relieving effect[1].
Phenidone, an orally active dual inhibitor of cyclooxygenase (COX) and lipoxygenase (LOX), ameliorates rat paralysis in experimental autoimmune encephalomyelitis. Phenidone is a potent hypotensive agent in the spontaneously hypertensive rat[1][2]. Phenidone is used as a photographic developer[3].
SC-236 is an orally active COX-2 specific inhibitor (IC50 = 10 nM) and a PPARγ agonist. SC-236 suppresses activator protein-1 (AP-1) through c-Jun NH2-terminal kinase. SC-236 exerts anti-inflammatory effects by suppressing phosphorylation of ERK in a murine model[1][2][3][4][5].
Flunixin-d3 is the deuterium labeled Flunixin. Flunixin Meglumine is a potent inhibitor of COX used as analgesic agent with anti-inflammatory and antipyretic activity[1][2].
Imrecoxib (BAP-909) is a novel and selective cyclooxygenase 2 (COX-2) inhibitor with an IC50 value of 18 nM, it also inhibits COX1- activity with an IC50 value of 115 nM. Imrecoxib (BAP-909) has anti-inflammatory effect[1].