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Monographs of Topical Drugs that Have Caused Contact Allergy/Allergic Contact Dermatitis
Published in Anton C. de Groot, Monographs in Contact Allergy, 2021
A 44-year-old man had been treated with an anti-inflammatory gel containing etofenamate for soreness on his right thigh, when, on the fourth day, itchy erythema, vesicles and exudation developed. He had not been exposed to sunlight. Patch tests were positive to the gel and to etofenamate 2% pet., but not to other NSAIDs including related anthranilic acid derivatives (8).
Laccase-Mediated Synthesis of Novel Antibiotics and Amino Acid Derivatives
Published in Peter Grunwald, Pharmaceutical Biocatalysis, 2019
3-Hydroxy-anthranilic acid and its derivatives react during laccase mediation to antibacterial phenoxazinone derivatives. These derivatives are homomolecular dimers type IV (Eq. 8.5). Laccase-mediated reaction of 3-hydroxy-anthranilic acid (15) and derivatives (16, 17) forming phenoxazinone derivatives (18 to 20) (Bruyneel et al., 2008; Eggert, 1997; Osiadacz et al., 1999).
Medications
Published in Gary W. Jay, Chronic Pain, 2007
There are over 20 different NSAIDs available in the United States in ten different chemical classes: Propionic acids (ibuprofen, naproxen, ketoprofen, ketorolac)Indoleacetic acids (indomethacin, sulindac, etodolac)Salicylic acids (nonacetylated)—sodium salsalate, choline magnesium, trisalicylate. Aspirin is acetylatedPhenylacetic acid (diclofenac)Naphthylalkanone (nabumetone)Oxicam (piroxicam)Anthranilic acid (enolic)—(mefenamic acid, meclofenamate)Pyrroleacetic acid (tolmetin)Pyrazolone (phenylbutazone)COX-2 inhibitors (celecoxib—rofecoxib and valdecoxib have been withdrawn from the market secondary to cardiovascular concerns)
Tryptophan 2,3-dioxygenase, a novel therapeutic target for Parkinson’s disease
Published in Expert Opinion on Therapeutic Targets, 2021
Fanni Annamária Boros, László Vécsei
The first step of the KP is the conversion of Trp into N-formyl-L-kynurenine in a reaction catalyzed by indoleamine 2,3-dioxygenase 1 and 2 (IDO1 and IDO2) and tryptophan 2,3-dioxygenase (TDO) enzymes. N-formyl-L-kynurenine is then metabolized into L-kynurenine (KYN) by formamidase. KYN is situated at an important branch point of the KP, since it can be converted into i) kynurenic acid (KYNA) by kynurenine aminotransferases (KATs), ii) anthranilic acid (AA) by kynureninase (KYNU), and iii) 3-hydroxykynurenine (3-HK) via a reaction catalyzed by kynurenine 3-monooxygenase (KMO). 3HK can further be metabolized into xanthurenic acid (XA) by KATs or can form 3-hydroxyanthranilate (3-HAA), which is further converted into 2-amino-3-carboxymuconate semialdehyde (ACMS) in a reaction catalyzed by 3-hydroxyanthranilate 3,4-dioxygenase. ACMS can be further processed by aminocarboxymuconate-semialdehyde decarboxylase (ACMSD) for the synthesis of 2-aminomuconate semialdehyde, which is then further metabolized into picolinic acid (PIC). ACMS can also undergo non-enzymatic cyclization and form quinolinic acid (QUIN), which is then ultimately metabolized into nicotinamide adenine dinucleotide (NAD+), a crucial molecule for cellular energy production and metabolism.
Solubility enhancement of mefenamic acid by inclusion complex with β-cyclodextrin: in silico modelling, formulation, characterisation, and in vitro studies
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2021
Dounia Sid, Milad Baitiche, Zineb Elbahri, Ferhat Djerboua, Mokhtar Boutahala, Zouhair Bouaziz, Marc Le Borgne
Mefenamic acid (MA), 2-[(2,3-dimethylphenyl)amino]benzoic acid, was selected as a drug model for our study. It is a potent non-steroidal anti-inflammatory drug (NSAID) of the anthranilic acid class. Moreover, it shows preferential inhibition of cyclo-oxygenase-2 (COX-2), inhibiting the action of prostaglandin synthetase19–21. Furthermore, MA is approved by the food and drug administration (FDA) in 196522. Due to its low solubility in water and high permeability in the gastrointestinal (GI) tract, MA is classified in the biopharmaceutics classification system (BCS) as class II drug23,24. It is widely indicated for inflammatory diseases and also as an analgesic for the treatment of musculoskeletal, osteoarthritis, rheumatoid arthritis, menstrual symptoms, and headach19,25–27. Furthermore, MA has been shown to have therapeutic effects in neurodegenerative disease (e.g. Alzheimer disease)28. In addition, MA, like other anti-inflammatory drugs, is emerging as new chemopreventive agents against cancer29. However, due to its low water solubility, high doses (250 or 500 mg twice a day administration) and side effects, mainly related to GI adverse consequences, including bleeding, ulceration or colitis lesions, and steatorrhoea, which can be sometimes fatal, made the use of MA limited19,30–32.
Clostridium botulinum neurotoxin A induces apoptosis and mitochondrial oxidative stress via activation of TRPM2 channel signaling pathway in neuroblastoma and glioblastoma tumor cells
Published in Journal of Receptors and Signal Transduction, 2020
Orhan Akpınar, Ahmet Özşimşek, Mustafa Güzel, Mustafa Nazıroğlu
Natural expressions of TRPM2 without DNA transfection were recently reported in the DBTRG glioblastoma and SH-SY5Y neuroblastoma cells [14–16]. The DBTRG and SH-SY5Y cells were divided into four groups as follows:Control group: The DBTRG and SH-SY5Y cells were kept in a cell culture medium for 24 h.BTX group: The DBTRG and SH-SY5Y cells were incubated with 5 IU BTX (Botox-100, Allergan Drugs Inc., Istanbul, Turkey) for 24 h [26].BTX + ACA group: After 24 h incubation of BTX, the DBTRG and SH-SY5Y cells were further incubated with 25 µM N-(p-amylcinnamoyl) anthranilic acid (ACA) for 30 min [24].BTX + 2-APB group: After 24 h incubation of BTX, the DBTRG and SH-SY5Y cells were incubated with 100 µM 2-aminoethyl diphenylborinate (2-APB) for 30 min [24].