Specific Disease Conditions
Harold G. Koenig in Chronic Pain, 2013
Sumatriptan and related drugs have contributed enormously to the treatment of migraine headache. They are highly effective in reducing or eliminating the pain, and can be administered by many different routes (orally, nasally, or by subcutaneous injection). Unfortunately, the “triptans” are quite expensive. In the long run, however, they may actually save money because they help to reduce the frequency of emergency-room and doctor visits. The biggest concern with these drugs, however, is they produce vasoconstriction in all blood vessels of the body, including the coronary arteries and cerebral arteries. Consequently, side effects include tightness of chest, paresthesias, and flushing, and the drug is contraindicated in patients with coronary artery disease, history of stroke, or peripheral vascular disease. Sumatriptan is available in 25 and 50 mg tablets, and 50 mg is the recommended single dose, with up to 300 mg per day if necessary (but no more).
Pharmacological Characterization of 5-Hydroxytryptamine Receptors in the Gastrointestinal Tract
T.S. Gaginella, J.J. Galligan in SEROTONIN and GASTROINTESTINAL FUNCTION, 2020
The only well-defined agonist at the 5-HT1D receptor is sumatriptan, where it is approximately 10 times less potent than 5-HT.9 Sumatriptan has approximately 10-fold selectivity for the 5-HT1D over the rat 5-HT1B receptor and demonstrates approximately 10- to 50-fold selectivity for 5-HT1D receptors over 5-HT1A receptors.53 This situation may be further complicated by recent reports that sumatriptan shows some binding affinity for the newest members of the 5-HT receptor family, which have been identified through molecular biological techniques.54,55 Whether this translates to functional activity has still to be demonstrated. When used in vivo it should be noted that sumatriptan only poorly penetrates the blood-brain barrier.
Helping You Understand Dr. Goldstein's Book
Katie Courmel in A Companion Volume to Dr. Jay A. Goldstein's Betrayal by the Brain, 2013
Sumatriptan is an agonist at the 5-HT1D serotonin receptor. It probably acts there to stop the release of peptides involved in the neurogenic inflammatory response that defines a migraine headache. Sumatriptan may directly block trigeminal nerve transmission, and it may be a dysfunction in the neural transmission through the trigeminovascular system that causes migraines. In neurosomatic patients, sumatriptan causes an increase in growth hormone and a tripling of neuropeptide Y (NPY) levels. Anatomically, sumatriptan may alter a complex neural network comprising the trigeminal nerve, locus ceruleus, reticular formation, and dorsal raphe nucleus to decrease diffuse pain and increase the signal-to-noise ratio. Symptomatically, neurosomatic patients may experience a decrease in pain with sumatriptan. A lucky few may experience total amelioration of their symptoms. When it is effective in eliminating CFS/FMS symptoms, sumatriptan produces global cerebral hypoperfusion, just as all other successful agents.
Intranasal drug delivery of sumatriptan succinate-loaded polymeric solid lipid nanoparticles for brain targeting
Published in Drug Development and Industrial Pharmacy, 2022
Rakesh Kumar Yadav, Kamal Shah, Hitesh Kumar Dewangan
Sumatriptan succinate (SS), a 5-hydroxytryptaminereceptor (5-HT1B/5-HT1D) agonist, was the first medicine licensed by the US Food and Drug Administration for the treatment of acute migraine in 1991. Its pharmacological action is mediated through vasoconstriction of the meningeal arteries, restriction of neurotransmitter release from neurons in the brain, suppression of nociceptive transmission, and reduction of trigeminal nerve activity. Sumatriptan is hydrophilic in nature and has been observed to pass the BBB to some amount in its basic form. SS is poorly absorbed and passes through a pre-systemic metabolic process. As a result, it has a limited oral bioavailability of roughly 15%. It has a plasma half-life of 1.5 h and an elimination half-life of 2.5 h, respectively [8,9]. The goal of this study was to create solid lipid nanoparticles (SLNPs) containing SS for nasal delivery to the brain. To improve the entrapment efficiency of hydrophilic drugs, a solvent injection approach was adopted and optimized by central composite design (CCD) model. Further, prepared formulation was evaluated for surface morphology, Fourier-transform infrared (FTIR) spectroscopy, in vitro release, histopathology, and brain targeting.
Treating status migrainosus in the emergency setting: what is the best strategy?
Published in Expert Opinion on Pharmacotherapy, 2018
László Vécsei, Délia Szok, Aliz Nyári, János Tajti
The possible routes of administration of triptans is numerous, including oral, SC, nasal spray, patch, transdermal iontophoresis, and rectal routes. In the ED setting, among parenteral formulations, the SC route is recommended as first choice regarding the way of application of triptans. Before administration of triptans, ECG should be performed to look for ischemic signs [20]. In a severe and long-lasting or recurrent migraine headache, SC sumatriptan (6 mg) should be offered (level B) (Figure 2(b)) [35]. Common adverse events of SC sumatriptan application are chest tightness, rash at injection site, generalized weakness, and dizziness [35]. Contraindications of triptans are cardiovascular diseases, uncontrolled hypertension, and pregnancy [12].
Sumatriptan improves the locomotor activity and neuropathic pain by modulating neuroinflammation in rat model of spinal cord injury
Published in Neurological Research, 2021
Khashayar Afshari, Amir Dehdashtian, Nazgol-Sadat Haddad, Seyedeh Zarifeh Jazaeri, Daniel C. Ursu, Mina Khalilzadeh, Arvin Haj-Mirzaian, Saeed Shakiba, Terry C Burns, Seyed Mohammad Tavangar, Mehdi Ghasemi, Ahmad Reza Dehpour
Sumatriptan is a selective 5-HT1B/D agonist widely used for migraine headache abortive treatment [35]. Activation of 5-HT1B/D receptors effectively inhibits cerebrovascular neurogenic inflammation [36]. Administration of sumatriptan exerts neuroprotective effects in cerebral ischemia, presumably mediated by 5-HT1D receptor agonism [15]. Moreover, sumatriptan inhibits the release of pathogenic and oxidative factors such as free radicals and NO in several in vivo and in vitro models of migraine and NP [16,37,38]. The inflammatory reaction of active microglia after SCI is predominantly dependent on these inflammatory markers, and TNF-α and IL-1β are known as two essential hallmarks for microglial inflammatory reaction [39]. Our results showed that sumatriptan markedly reduced the cord tissue levels of these inflammatory cytokines, leading to decreased activation and infiltration of immune cells associated with the relatively lower presence of neuronal vacuolation and cyst formation at the site of injury. Additionally, there is evidence that the vasospasm induced by sumatriptan reduces the haemorrhage after SCI [40]. These effects are indicative of the inhibition of the secondary mechanism of injury in SCI resulting in significant improvement of the locomotor activity and attenuation of NP [4,41]. In fact, the therapeutic effects of sumatriptan in this study rivalled that of minocycline, a neuroprotective agent known to have significant potency in the treatment of SCI by attenuation of neuroinflammation and microglial activity which could be mediated by the inhibition of pro-inflammatory mediators, i.e. TNF-α and IL-1β [23,24,27].
Related Knowledge Centers
- Chest Pain
- Cluster Headache
- Serotonin Syndrome
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- Migraine
- Oral Administration
- Nasal Administration
- Subcutaneous Administration
- 5-Ht1B Receptor
- 5-Ht1D Receptor