Sumatriptan Succinate - CAS 103628-48-4
Catalog number: 103628-48-4
Category: Inhibitor
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Molecular Formula:
Molecular Weight:
5-HT Receptor
Sumatriptan Succinate is a triptan sulfa drug containing a sulfonamide group for the treatment of migraine headaches.
GR 43175; GR43175; GR-4317
Canonical SMILES:
1.Migraine-tic syndrome: Two further case reports.
Hinze S1, Davies P2, Astbury T2, Lane R3. Cephalalgia. 2016 Apr 7. pii: 0333102416644436. [Epub ahead of print]
BACKGROUND: Migraine-tic syndrome was first reported in 2004 in a 44-year-old woman who had concomitant symptoms of both typical trigeminal neuralgia and migraine. We report here two further cases of migraine-tic syndrome and speculate on the relevance of this condition to the pathophysiology of headache.
2.In-vitro characterization of buccal iontophoresis: the case of sumatriptan succinate.
Telò I1, Tratta E1, Guasconi B1, Nicoli S1, Pescina S1, Govoni P2, Santi P1, Padula C3. Int J Pharm. 2016 Apr 22. pii: S0378-5173(16)30337-4. doi: 10.1016/j.ijpharm.2016.04.054. [Epub ahead of print]
Buccal administration of sumatriptan succinate might be an interesting alternative to the present administration routes, due to its non-invasiveness and rapid onset of action, but because of its low permeability, a permeation enhancement strategy is required. The aim of this work was then to study, in vitro, buccal iontophoresis of sumatriptan succinate. Permeation experiments were performed in vitro across pig esophageal epithelium, a recently proposed model of human buccal mucosa, using vertical diffusion cells. The iontophoretic behavior of the tissue was characterized by measuring its isoelectric point (Na+ transport number and the electroosmotic flow of acetaminophen determination) and by evaluating tissue integrity after current application. The results obtained confirm the usefulness of pig esophageal epithelium as an in-vitro model membrane for buccal drug delivery. The application of iontophoresis increased sumatriptan transport, proportionally to the current density applied, without tissue damage: electrotransport was the predominant mechanism.
3.Development and validation of an LC-ESI-MS/MS method for the simultaneous quantification of naproxen and sumatriptan in human plasma: application to a pharmacokinetic study.
Brêtas JM1, César IC2, Brêtas CM1, Teixeira LS3, Bellorio KB3, Mundim IM3, Pianetti GA1. Anal Bioanal Chem. 2016 Mar 28. [Epub ahead of print]
A sensitive and fast liquid chromatography-electrospray ionization tandem mass spectrometry (LC-ESI-MS/MS) method was developed and validated for the simultaneous quantification of naproxen and sumatriptan in human plasma. A simple liquid-liquid extraction procedure, with a mixture of ethyl acetate, methyl tert-butyl ether, and dichloromethane (4:3:3, v/v), was used for the cleanup of plasma. Naratriptan and aceclofenac were employed as internal standards. The analyses were carried out using an ACE C18 column (50 × 4.6 mm i.d.; particle size 5 μm) and a mobile phase consisting of 2 mM aqueous ammonium acetate with 0.025 % formic acid and methanol (38:62, v/v). A triple-quadrupole mass spectrometer equipped with an electrospray source in the positive mode was set up in the selective reaction monitoring mode to detect the ion transitions m/z 231.67 → m/z 185.07, m/z 296.70 → m/z 157.30, m/z 354.80 → m/z 215.00, and m/z 336.80 → m/z 97.94 for naproxen, sumatriptan, aceclofenac, and naratriptan, respectively.
4.Gi-Protein Coupled 5-HT1B/D Receptor Agonist Sumatriptan Induces Type I Hyperalgesic Priming.
Araldi D1, Ferrari LF, Levine JD. Pain. 2016 Apr 12. [Epub ahead of print]
We have recently described a novel form of hyperalgesic priming (type II) induced by agonists at two clinically important Gi-protein coupled receptors (Gi-GPCRs), mu-opioid and A1-adenosine. Like mu-opioids, the anti-migraine triptans, which act at 5-HT1B/D Gi-GPCRs have been implicated in pain chronification. We determined if sumatriptan, a prototypical 5-HT1B/D agonist produces type II priming. Characteristic of hyperalgesic priming, intradermal injection of sumatriptan (10 ng) induced a change in nociceptor function such that a subsequent injection of prostaglandin-E2 (PGE2) induces prolonged mechanical hyperalgesia. However, onset to priming was delayed 3 days, characteristic of type I priming. Also characteristic of type I priming, a protein kinase Cε (PKCε), but not a PKA inhibitor attenuated the prolongation phase of PGE2 hyperalgesia. The prolongation of PGE2 hyperalgesia was also permanently reversed by intradermal injection of cordycepin, a protein translation inhibitor.
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CAS 103628-48-4 Sumatriptan Succinate

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