Medicine

α5IA (LS-193,268) is a nootropic drug invented in 2004 by a team working for Merck, Sharp and Dohme, which acts as a subtype-selective inverse agonist at the benzodiazepine binding site on the GABAA receptor. It binds to the α1, α2, α3 and α5 subtypes, but shows much higher efficacy at the α5 subtype, and acts either as a weak partial agonist or inverse agonist at the other subtypes, with its partial agonist effect at α2 likely to be responsible for the lack of anxiety produced by this drug when compared to older α5-preferring inverse agonists such as L-655,708.[1][2]

The α5 subtype is expressed predominantly in the hippocampus, an area of the brain involved with learning and memory, and activation of this subtype is thought to be largely responsible for producing the cognitive side effects displayed by many benzodiazepine and nonbenzodiazepine drugs, such as amnesia and difficulties with learning and memory. This led researchers to conclude that a drug acting as an inverse agonist at this subtype should have the opposite effect and enhance learning and memory.[3][4]

Older non-selective inverse agonists at the benzodiazepine site such as DMCM are associated with a range of other effects including anxiety and convulsions, but because α5IA acts specifically at the α5 subtype it produces nootropic effects in animal studies, yet without any significant anxiogenic or pro-convulsant effects. This gives α5IA the potential to be a useful drug either to be used alongside benzodiazepines to counteract their cognitive side effects, or by itself as a nootropic with possible applications in the treatment of Alzheimer’s disease and other forms of dementia.[5][6]

α-Methyl-5-hydroxytryptamine (α-Methyl-5-HT) is a tryptamine drug and research chemical closely related to the neurotransmitter serotonin (5-hydroxytryptamine, 5-HT). It acts as a moderately selective full agonist at the 5-HT2 receptors, having the highest affinity for 5-HT2B and the lowest affinity for 5-HT2A.[1][2][3]

Zylofuramine is a stimulant drug. It was developed in 1961,[1] and was intended for use as an appetite suppressant and for the treatment of senile dementia in the elderly, but there is little information about it and it does not appear to have ever been marketed.[2]

Zylofuramine is legal throughout the world. Its chemical structure has a vague similarity to other N-ethyl substituted stimulant drugs such as ethylamphetamine, but its structure would probably not be close enough for it to be considered a controlled substance analogue.

The most common side effect of Zotepine is weight gain. This weight gain side effect compares badly to the older typical antipsychotics. Somnolence is the second most common side effect. Constipation, asthenia, dry mouth, and akathisia are also reported.

The likelihood of side effects are as follows:

Weight gain: Medium to high Hyperprolactinemia: high Sexual problems: high Sedation: high EPSE’s (Assumes that normal doses are used but may vary with the dose given):Low Hypotension: Medium Hyperglycaemia: Low

Pharmacology

The antipsychotic effect of zotepine is thought to be mediated through antagonist activity at dopamine and serotonin receptors. Zotepine has a high affinity for the dopamine D1 and D2 recepetors. It also affects the 5HT2a, 5HT2c, 5HT6, and 5HT7 receptors. In addition, it inhibits the reuptake of noradrenaline. It is thought that this is why zotepine has a high efficacy for the negative symptoms of schizophrenia.

Zotepine (Nipolept, Losizopilon, Lodopin, Setous) is an atypical antipsychotic indicated for acute and chronic schizophrenia. It has been used in Germany since 1990 and Japan since 1982.

The most common dosage used is 150 mg daily. It is suggested that zotepine therapy starts at 75 mg to 150 mg divided into three daily doses. Some people may need to have their dosage increased to 300 mg.

Zosuquidar is a compound of antineoplastic drug candidates currently under development. It is now in “Phase 3″ of clinical tests in the United States. Its action mechanism consists of the inhibition of P-glycoproteins; other drugs with this mechanism include tariquidar and laniquidar. P-glycoproteins are proteins which convert the energy derived from the hydrolysis of ATP to structural changes in protein molecules, in order to perform coupling, thus discharging medicine from cells. If P-glycoprotein coded with the MDR1 gene manifests itself in cancer cells, it discharges much of the antineoplastic drugs from the cells, making cancer cells medicine tolerant, and rendering antineoplastic drugs ineffective. This protein also manifests itself in normal organs not affected by the cancer (such as the liver, small intestine, and skin cells in blood vessels of the brain), and participates in the transportation of medicine. The compound Zosuquidar inhibits this P-glycoprotein, causing the cancer cells to lose their medicine tolerance, and making antineoplastic drugs effective.

Zorubicin (INN) is an anthracycline.

Zoopharmacognosy refers to the process by which animals self-medicate, by selecting and using plants, soils, and insects to treat and prevent disease. Coined by Dr. Eloy Rodriguez, a biochemist and professor at Cornell University, the word is derived from roots zoo (”animal”), pharma (”drug”), and gnosy (”knowing”).[1]

Observers have noticed that some species ingest non-foods, such as toxic plants, clay or charcoal, to ward off parasitic infestation or poisoning.[2] For example, Jane Goodall has seen chimpanzees eating certain bushes to make themselves sick. Some Brazilian parrots eat kaolin (a form of clay).

Illustrating the medicinal knowledge of some species, apes have been observed selecting a particular part of a medicinal plant by taking off leaves, then breaking the stem to suck out the juice.[3] In an interview with Neil Campbell, Rodriguez describes the importance of biodiversity to medicine:
Some of the compounds we’ve identified by zoopharmacognosy kill parasitic worms, and some of these chemicals may be useful against tumors. There is no question that the templates for most drugs are in the natural world.[3]

Two observations have been made by William Astor regarding the self-medicative behavior of Estrildid finches of several species:[4] 1. Estrildid finches in captivity of several different species have been observed to correctly target appropriate antibiotics out of a range made available to them through which they were able to cure themselves of life threatening diseases ( as opposed to relatively minor ailments like indigestion.) 2. Estrildid finches in captivity of several different species do not learn this self-medicative behavior from their parents or others in the flock through social learning like apes and chimpanzees are suspected of doing. This ability of Estrildid finches seems to be innate but as to how they can do it is a complete mystery.

A female capuchin monkey in captivity was observed using tools covered in a sugar-based syrup to groom her wounds and those of her infant.[5][

The Zomig ZMT dissolvable pill contains aspartame, and should be avoided by anyone sensitive to that ingredient.

Serious cardiac events, including myocardial infarction, have been associated with zolmitriptan. These are, however, rare.

Reported minor adverse reactions include: hypesthesia, paresthesia (all types), warm and cold sensations, chest pain, throat and jaw tightness, dry mouth, dyspepsia, dysphagia, nausea, somnolence, vertigo, asthenia, myalgia, myasthenia and sweating.