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Skeletal formula
Ball-and-stick model
Clinical data
Trade namesOlbetam
AHFS/Drugs.comUK Drug Information
Routes of
ATC code
Legal status
Legal status
  • UK: POM (Prescription only)
Pharmacokinetic data
Protein bindingNone
Elimination half-lifePhase 1: 2 hrs
Phase 2: 12–14 hrs
  • 5-Carboxy-2-methyl-1-oxidopyrazin-1-ium
CAS Number
PubChem CID
CompTox Dashboard (EPA)
ECHA InfoCard100.051.736 Edit this at Wikidata
Chemical and physical data
Molar mass154.125 g·mol−1
3D model (JSmol)
  • [O-][n+]1c(cnc(C(=O)O)c1)C
  • InChI=1S/C6H6N2O3/c1-4-2-7-5(6(9)10)3-8(4)11/h2-3H,1H3,(H,9,10) checkY

Acipimox (trade name Olbetam in Europe) is a niacin derivative used as a lipid-lowering agent. It reduces triglyceride levels and increases HDL cholesterol. It may have less marked adverse effects than niacin, although it is unclear whether the recommended dose is as effective as standard doses of niacin.


Contraindications are peptic ulcers, acute bleeding, recent heart attack, acute decompensated heart failure, and severe chronic kidney disease.[1]

Adverse effects

As with niacin and related drugs, the most common adverse effects are flushing (associated with prostaglandin D2[2]) and gastrointestinal disturbances such as indigestion, which occur in at least 10% of patients.[1] Flushing can be reduced by taking aspirin 20 to 30 minutes before taking acipimox. Palpitations have also been described.[citation needed] High doses can cause headache,[3] and precipitate gout.[citation needed] In contrast to niacin, no impairment of glucose tolerance and no disorders of liver function have been found in studies, even under high doses of acipimox.[1][3]


No interactions with other drugs are known. Theoretically, combination with statins and fibrates could increase the incidence of myalgia. Alcohol can increase the risk of flushing.[1][3]


Mechanism of action

Like niacin, acipimox acts on the niacin receptor 1, inhibiting the enzyme triglyceride lipase. This reduces the concentration of fatty acids in the blood plasma and their inflow into the liver. Consequently, VLDL cholesterol production in the liver is reduced, which leads indirectly to a reduction in LDL and increase in HDL cholesterol.[1][2]


Acipimox is completely absorbed from the gut. It is not bound to blood plasma proteins and not metabolized. Elimination occurs in two phases, the first having a half-life of two hours, the second of 12 to 14 hours. The substance is eliminated via the kidney.[1]


  1. ^ a b c d e f Haberfeld H, ed. (2015). Austria-Codex (in German). Vienna: Österreichischer Apothekerverlag.
  2. ^ a b Benyó Z, Gille A, Kero J, Csiky M, Suchánková MC, Nüsing RM, et al. (December 2005). "GPR109A (PUMA-G/HM74A) mediates nicotinic acid-induced flushing". The Journal of Clinical Investigation. 115 (12): 3634–40. doi:10.1172/JCI23626. PMC 1297235. PMID 16322797.
  3. ^ a b c Dinnendahl V, Fricke U, eds. (1989). Arzneistoff-Profile (in German). Vol. 1 (6 ed.). Eschborn, Germany: Govi Pharmazeutischer Verlag. ISBN 978-3-7741-9846-3.