Gaboxadol, also known as 4,5,6,7-tetrahydroisoxazolo(5,4-c)pyridin-3-ol (THIP), is a conformationally constrained derivative of the alkaloid muscimol (a constituent of Amanita muscaria) that was first synthesized in 1977 by the Danish chemist Povl Krogsgaard-Larsen.

[1] It was not until 1996 that researchers attempted to harness gaboxadol's frequently reported sedative "adverse effect" for the treatment of insomnia, resulting in a series of clinical trials sponsored by Lundbeck and Merck.

[1][2] In March 2007, Merck and Lundbeck cancelled work on the drug, citing safety concerns and the failure of an effectiveness trial.

Unlike benzodiazepines, gaboxadol does not demonstrate reinforcement in mice or baboons despite activation of dopaminergic neurons in the ventral tegmental area.

[8] The supra-maximial efficacy of gabaxadol at α4β3δ GABAA receptors has been attributed to an increase in the duration and frequency of channel openings relative to the endogenous agonist GABA.