Cotinine

Cotinine ((-) -Cotinine) is an orally active alkaloid found in tobacco and is the primary metabolite of nicotine. Cotinine is metabolized by CYP2A13 into trans-3'-hydroxycotinine. Cotinine is used as a biomarker to measure exposure to tobacco smoke components. Cotinine has vasodepressor activity. The mixture of cotinine and nicotine (Nicotine) has antiproliferative activity against pterygium. (S) - (-) -Cotinine activates nicotinic acetylcholine receptors (nAChR) in a calcium-dependent manner, leading to the release of dopamine (Dopamine, HY-B0451) . Cotinine ((-) -Cotinine) is used in research related to cardiovascular and inflammatory diseases[1][2][3][4][5].

Product Specifications

CAS Number

[486-56-6]

Product Name Alternative

(-) -Cotinine; (S) -Cotinine; NIH-10498

UNSPSC

12352005

Hazard Statement

H302, H315, H319, H335

Target

Endogenous Metabolite; nAChR

Type

Natural Products

Related Pathways

Membrane Transporter/Ion Channel; Metabolic Enzyme/Protease; Neuronal Signaling

Field of Research

Inflammation/Immunology; Cardiovascular Disease

Assay Protocol

https://www.medchemexpress.com/Cotinine.html

Purity

99.98

Solubility

DMSO : 65 mg/mL (ultrasonic) |Ethanol : 120 mg/mL (ultrasonic)

Smiles

O=C1N(C)[C@H](C2=CC=CN=C2)CC1

Molecular Formula

C10H12N2O

Molecular Weight

176.22

Precautions

H302, H315, H319, H335

References & Citations

[1]Dolcini MM, et al. An assessment of the validity of adolescent self-reported smoking using three biological indicators. Nicotine Tob Res. 2003 Aug;5 (4) :473-83.|[2]Sastry BV, et al. Distribution and retention of nicotine and its metabolite, cotinine, in the rat as a function of time. Pharmacology. 1995 Feb;50 (2) :128-36.|[3]Borzelleca J F, et al. Studies on the respiratory and cardiovascular effects of (-) -cotinine[J]. Journal of Pharmacology and Experimental Therapeutics, 1962, 137 (3) : 313-318.|[4]Dwoskin L P, et al. (S) - (−) -Cotinine, the major brain metabolite of nicotine, stimulates nicotinic receptors to evoke [3H] dopamine release from rat striatal slices in a calcium-dependent manner[J]. Journal of pharmacology and experimental therapeutics, 1999, 288 (3) : 905-911.|[5]Yang Q, et al. Continuous exposure of nicotine and cotinine retards human primary pterygium cell proliferation and migration.