Skeletal formula
Ball-and-stick model
Clinical data
Trade names Olbetam
AHFS/ UK Drug Information
Routes of
ATC code C10AD06 (WHO)
Legal status
Legal status
  • UK: POM (Prescription only)
Pharmacokinetic data
Bioavailability 100%
Protein binding None
Metabolism None
Biological half-life Phase 1: 2 hrs
Phase 2: 12–14 hrs
Excretion Renal
CAS Number 51037-30-0 YesY
PubChem (CID) 5310993
ChemSpider 4470534 YesY
KEGG D07190 YesY
Chemical and physical data
Formula C6H6N2O3
Molar mass 154.13 g·mol−1
3D model (Jmol) Interactive image

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, fresh myocardial infarction, acute decompensated heart failure, and severe renal insufficiency.[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. High doses can cause headache,[3] and precipitate gout. 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. 1 2 3 4 5 6 Haberfeld, H, ed. (2015). Austria-Codex (in German). Vienna: Österreichischer Apothekerverlag.
  2. 1 2 Benyó, Z; Gille, A; Kero, J; Csiky, M; Suchánková, M. C.; Nüsing, R. M.; Moers, A; Pfeffer, K; Offermanns, S (2005). "GPR109A (PUMA-G/HM74A) mediates nicotinic acid–induced flushing". Journal of Clinical Investigation. 115 (12): 3634–3640. doi:10.1172/JCI23626. PMC 1297235Freely accessible. PMID 16322797.
  3. 1 2 3 Dinnendahl, V; Fricke, U, eds. (1989). Arzneistoff-Profile (in German). 1 (6 ed.). Eschborn, Germany: Govi Pharmazeutischer Verlag. ISBN 978-3-7741-9846-3.
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