Alkaloid peptides are a group of naturally occurring chemical compounds containing mostly basic nitrogen atoms. Alkaloids peptides are generated by organisms such as bacteria, fungi, plants and animals as well. Most alkaloids can be extracted and purified by acid-base extraction. And many alkaloids peptides are toxic to other organisms. Alkaloids peptides often have pharmacological effects and can be used as medications and recreational drug or in entheogenic rituals. Typical examples of peptide alkaloid are: ergotamine, pandamine, dynorphin A-(1-8)-octapeptide, N beta-(D-Leu-D-Arg-D-Arg-D-Leu-D-Phe)-naltrexamine, etc. The applications of alkaloids peptides have covered the medical and agricultural fields. Alkaloids peptides play roles in a diversity of metabolic systems in humans and other animals .
Ergotamine is an ergopeptine and part of the ergot family of alkaloids; it is structurally and biochemically closely related to ergoline. It possesses structural similarity to several neurotransmitters, and has biological activity as a vasoconstrictor.
It is used medicinally for treatment of acute migraine attacks (sometimes in combination with caffeine). Medicinal usage of ergot fungus began in the 16th century to induce childbirth, yet dosage uncertainties discouraged the use. It has been used to prevent post-partum haemorrhage (bleeding after childbirth). It was first isolated from the ergot fungus by Arthur Stoll at Sandoz in 1918 and marketed as Gynergen in 1921.
The mechanism of action of ergotamine is complex. The molecule shares structural similarity with neurotransmitters such as serotonin, dopamine, and epinephrine and can thus bind to several receptors acting as an agonist. The anti-migraine effect is due to constriction of the intracranial extracerebral blood vessels through the 5-HT1B receptor, and by inhibiting trigeminal neurotransmission by 5-HT1D receptors. Ergotamine also has effects on the dopamine and norepinephrine receptors. Its side effects are due mainly to its action at the D2 dopamine and 5-HT1A receptors .
Ergotamine produces vasoconstriction peripherally as well as damages the peripheral epithelium. In high doses ergotamine is conducive to vascular stasis, thrombosis and gangrene. It can increase uterine contractivity and occasionally is used therapeutically immediately post-partum to decrease uterine bleeding. See also ergometrine. Ergotamine continues to be prescribed for migraines.
In recent years, the researchers pay more and more attention to the side effect of ergotamine. For example, Takotsubo cardiomyopathy (TC) is a recently increasing diagnosed disease showed by transient apical or mid-apical left ventricular dysfunction. It is known as a disease of postmenopausal women, which is usually triggered by emotional or physical stress. Although the trigger is mostly endogenous, some drugs have also been reported as the cause. Published case reports of TC associated with drug usage consist of sympathomimetic drugs, inotropic agents, thyroid hormone, cocaine, and 5-fluorouracil. Some researchers present an unusual case of TC in which the possible trigger is ergotamine toxicity .
Today, ergotamine has been used in clinic for a long time, even the treatment of AIDS, but the research on its side effects are more and more hot, a lot of the laboratory are studying its molecular mechanism, and Karebay can synthetic ergotamine with High purity.
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References:  Walkembach J, et al. (October 2005). “Interactions of metoclopramide and ergotamine with human 5-HT3A receptors and human 5-HT reuptake carriers”. Br. J. Pharmacol. 146 (4): 543–52.  Schardl CL, et al. (2006). “Ergot alkaloids–biology and molecular biology”. Alkaloids Chem. Biol. The Alkaloids: Chemistry and Biology 63: 45–86.  Ozpelit E, et al. Ergotamine-Induced Takotsubo Cardiomyopathy. Am J Ther. 2014 Aug 5.