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| Clinical data | |
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| Trade names | Proglycem, others |
| AHFS/Drugs.com | Monograph |
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| Routes of administration | By mouth,intravenous |
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| Pharmacokinetic data | |
| Protein binding | 90% |
| Metabolism | Liveroxidation andsulfate conjugation |
| Eliminationhalf-life | 21-45 hours |
| Excretion | Kidney |
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| CompTox Dashboard(EPA) | |
| ECHA InfoCard | 100.006.063 |
| Chemical and physical data | |
| Formula | C8H7ClN2O2S |
| Molar mass | 230.67 g·mol−1 |
| 3D model (JSmol) | |
| Melting point | 330 to 331 °C (626 to 628 °F) |
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Diazoxide, sold under the brand nameProglycem among others, is amedication used to treatlow blood sugar due to a number of specific causes.[4] This includesislet cell tumors that cannot be removed andleucine sensitivity.[4] It can also be used in refractory cases ofsulfonylurea toxicity.[5] It is takenby mouth.[4]
Diazoxide, used as the salt diazoxide choline, and sold under the brand nameVykat XR, is used for the treatment ofhyperphagia in people withPrader–Willi syndrome.[3] It was approved for this use in the United States in March 2025.[6]
Common side effects include high blood sugar, fluid retention,low blood platelets, a fast heart rate, increased hair growth, and nausea.[4] Other severe side effects includepulmonary hypertension andheart failure.[4] It is chemically similar tothiazide diuretics.[4] It works by decreasing insulin release from the pancreas and increasing glucose release by the liver.[4]
Diazoxide was approved for medical use in the United States in 1973.[4] It is on theWorld Health Organization's List of Essential Medicines.[7] It is available as ageneric medication.[8]
Diazoxide is used as avasodilator in the treatment of acutehypertension ormalignant hypertension.[9]
Diazoxide also inhibits the secretion ofinsulin by openingATP-sensitive potassium channel ofbeta cells of thepancreas; thus, it is used to counter hypoglycemia in disease states such asinsulinoma (a tumor producing insulin)[10] orcongenital hyperinsulinism.
Diazoxide acts as a positiveallosteric modulator of theAMPA andkainate receptors, suggesting potential application as a cognitive enhancer.[11]
Diazoxide interferes with insulin release through its action on potassium channels.[12] Diazoxide is one of the most potent openers of theK+ ATP channels present on the insulin producing beta cells of the pancreas. Opening these channels leads to hyperpolarization of cell membrane, a decrease in calcium influx, and a subsequently reduced release of insulin.[5]
The USFood and Drug Administration (FDA) published a safety announcement in July 2015 highlighting the potential for development ofpulmonary hypertension in newborns and infants treated with this drug.[13]
Diazoxide has been associated with development ofhypertrichosis and stimulation ofscalp hairgrowth.[14][15]
Diazoxide, formulated as itscholinesalt diazoxide choline, is an experimental antiobesity drug being tested in people withPrader-Willi syndrome[16][17][18] andmonogenic obesity caused by mutations in theSH2B1,PCSK1, orSIM1 genes.[19]
Other potassium channel openers, like diazoxide [39, 40] and pinacidil [41] can cause hypertrichosis in humans as well as minoxidil. In balding macaques minoxidil, cromakalin and P-1075 (a pinacidil analogue) stimulate hair growth in about 20 weeks of topical treatment, whereas a fourth potassium channel opener, called RP49356, is not effective [42].
The evidence that [potassium channel openers (PCOs)] are active on hair growth is correlative. In humans three PCOs have been reported to affect hair growth. Minoxidil was reported to induce hypertrichosis during early clinical trials as an antihypertensive [12]. These side effects were characterized by increasingly visual facial hair, thickening of eyebrows, and diffuse hair growth across the upper back and limbs. Systemic minoxidil induced hypertrichosis in 80–100% of adults [13]. Clinical trials using topical minoxidil demonstrate increased scalp hair in about 39% of treated balding men. Oral diazoxide causes hypertrichosis in most hypoglycemic children and about 1% of adults, and induces some scalp hair in 25% of the balding patients [13–15]. Systemic pinacidil induces hypertrichosis in 2–13% of patients [13]. We are not aware of any topical hair growth trials using pinacidil.
