Head-to-head clinical analysis & difference comparison: details on mechanism of action, dosing, half-life, interactions, and maternal-fetal safety.
TRIGLIDE vs NIACOR
Clinician-reviewed, head-to-head comparison of mechanism, dosing, pharmacokinetics, and safety profiles.
Last clinically reviewed: July 2026 · OpiCalc Medical Review Team
TRIGLIDE (fenofibrate) is a peroxisome proliferator-activated receptor alpha (PPARα) activator. It increases lipolysis and elimination of triglyceride-rich particles from plasma by activating lipoprotein lipase and reducing production of apolipoprotein C-III.
Niacin (nicotinic acid) reduces VLDL and LDL synthesis by inhibiting lipolysis in adipose tissue, decreasing free fatty acid flux to the liver, and inhibiting hepatic triglyceride synthesis. It also increases HDL by reducing catabolism of apolipoprotein A-I.
Adjunctive therapy to diet for severe hypertriglyceridemia (Fredrickson types IV and V),Primary hypercholesterolemia or mixed dyslipidemia (Fredrickson types IIa and IIb)
Adjunct to diet for reduction of elevated total cholesterol, LDL-C, apo B, and triglyceride levels, and to increase HDL-C in primary hypercholesterolemia and mixed dyslipidemia,Adjunct to diet for reduction of risk of recurrent myocardial infarction in patients with coronary artery disease and hypercholesterolemia,Adjunct to diet for slowing progression of coronary atherosclerosis,Off-label: treatment of pellagra (niacin deficiency)
Initial dose: 60 mg (1 tablet) twice daily, gradually increased over 3-7 days to maintenance dose of 120 mg twice daily.
Initial: 250 mg orally once daily after evening meal; titrate up by 250–500 mg/day every 2–4 weeks. Maintenance: 1–2 g/day in divided doses (2–3 times daily). Maximum: 6 g/day.
22-35 hours; prolonged in renal impairment (up to 50 hours).
20–45 minutes for immediate-release niacin; terminal half-life of main metabolites (nicotinuric acid) is approximately 1.5–4 hours; short half-life necessitates multiple daily dosing for lipid effects
Fenofibrate is a prodrug that is rapidly hydrolyzed by esterases to the active metabolite fenofibric acid. Fenofibric acid is conjugated with glucuronic acid and excreted in urine. Major CYP450 involvement is minimal; however, fenofibric acid is a substrate of CYP3A4 and to some extent CYP2C8.
Hepatic metabolism via two pathways: conjugation with glycine to form nicotinuric acid (major, low-affinity high-capacity) and oxidation to N-methylnicotinamide and other metabolites (minor, high-affinity low-capacity). Enzymes involved: nicotinamide N-methyltransferase (NNMT) and aldehyde oxidase.
Primarily renal (70% as unchanged drug), 20% fecal, <10% biliary.
Renal: 60-88% as unchanged drug and metabolites after oral administration; fecal: <2%
>99% to albumin.
<20% bound to albumin; minimal binding to other plasma proteins
0.11-0.16 L/kg; indicates limited extravascular distribution.
0.5–0.7 L/kg; indicates distribution into total body water and some tissue binding
60-70% (oral).
Oral immediate-release: 60–76% (variable due to first-pass metabolism); sustained-release: lower bioavailability (50–60%) due to increased presystemic metabolism
No specific dose adjustment for GFR >10 m L/min; avoid use in patients with GFR <10 m L/min or on dialysis.
No specific adjustment recommended; use caution in severe renal impairment (Cr Cl <30 m L/min) due to potential accumulation; consider reducing dose or prolonging interval.
Contraindicated in Child-Pugh class B and C; use with caution in Child-Pugh class A with dose reduction (e.g., 60 mg twice daily) and monitor closely.
Contraindicated in Child-Pugh class B and C; use with caution in mild impairment (Child-Pugh A) with dose reduction of 50% initially.
Not approved for pediatric patients; safety and efficacy not established.
For hyperlipidemia (off-label): Initial 50–100 mg/kg/day orally divided into 2–3 doses; titrate over 4–6 weeks up to 200–300 mg/kg/day; maximum 6 g/day. Not recommended in children <2 years.
Use lowest effective dose; monitor for cardiac and electrolyte disturbances; start at 60 mg twice daily and titrate slowly.
Start at lowest dose (250 mg daily); titrate slowly due to increased risk of flushing, hypotension, and hepatotoxicity; monitor liver function and glucose closely.
None
None.
Hepatotoxicity: elevations in serum transaminases, rare reports of hepatitis and cirrhosis; monitor hepatic function,Cholelithiasis: increased cholesterol excretion into bile, risk of gallstone formation,Rhabdomyolysis: increased risk in patients with renal impairment, hypothyroidism, or those taking statins or other fibrates,Pancreatitis: observed in patients with severe hypertriglyceridemia,Renal impairment: contraindicated in severe renal disease; dose adjustment needed in mild-to-moderate impairment
Hepatotoxicity: elevated liver enzymes, hepatitis; discontinue if persistent elevations occur,Flushing: prostaglandin-mediated, can be reduced by taking aspirin prior; tolerance develops,Hyperuricemia: may precipitate gout,Hyperglycemia: may increase blood glucose; use with caution in diabetes,Peptic ulcer disease: reactivation may occur,Hypotension: can occur, especially with vasoactive drugs
Severe renal impairment (e GFR < 30 m L/min/1.73 m²),Active liver disease including primary biliary cirrhosis and unexplained persistent liver function abnormalities,Known gallbladder disease,Hypersensitivity to fenofibrate or any component of the formulation,Nursing mothers (due to potential for tumorigenicity in animal studies)
Hypersensitivity to niacin or any component of formulation,Significant or unexplained hepatic dysfunction,Active peptic ulcer disease,Arterial hemorrhage
Take with food to enhance bioavailability. Avoid high-fat meals that may exacerbate hypertriglyceridemia. Limit alcohol intake as it can increase triglyceride levels and hepatotoxicity risk. Grapefruit juice has no significant interaction with fenofibrate.
Avoid high-fat meals as they may increase risk of flushing. Take with low-fat snack. Alcohol and hot drinks can exacerbate flushing.
TRIGLIDE (fenofibrate) is contraindicated in pregnancy due to potential fetal harm. First trimester: no adequate human data; animal studies show embryotoxicity and delayed ossification at doses below human exposure. Second and third trimesters: risk of fetal skeletal abnormalities and growth retardation; use only if maternal benefit outweighs risk.
FDA Pregnancy Category C. Niacin is not recommended for use in pregnant women due to potential fetal harm, though no well-controlled studies exist. In animal studies, high doses have caused fetal abnormalities. First trimester: Avoid use due to theoretical risk of teratogenicity. Second and third trimesters: Use only if clearly needed, as niacin can cause vasodilation and potential hypotension, which may reduce uteroplacental perfusion.
Fenofibrate is excreted in rat milk; no human data. M/P ratio unknown. Breastfeeding is contraindicated due to potential lipid metabolism disruption in infant and lack of safety data.
Niacin is excreted into human breast milk in minimal amounts; M/P ratio unknown. The American Academy of Pediatrics considers niacin compatible with breastfeeding. However, high maternal doses may lead to adverse effects in the infant due to potential accumulation. Caution is advised; monitor infant for flushing or gastrointestinal disturbances.
No dose adjustment guidelines due to contraindication. Pharmacokinetics in pregnancy not studied; no recommended dose changes.
No specific dose adjustments recommended due to lack of pharmacokinetic studies in pregnant women. However, physiological changes in pregnancy (increased plasma volume, renal clearance) may reduce niacin levels, potentially requiring dose increase. Use the lowest effective dose and avoid extended-release formulations due to higher hepatotoxicity risk. Usual adult doses (500-2000 mg/day) may be used with caution.
TRIGLIDE (fenofibrate) is a fibric acid derivative used as adjunctive therapy to diet for severe hypertriglyceridemia (≥500 mg/d L) to reduce risk of pancreatitis. Monitor renal function before initiation; dose adjustment required if e GFR 30-59 m L/min (starting dose: 48 mg/day). Avoid use if e GFR <30 m L/min or active liver disease. Coadministration with statins increases risk of myopathy/rhabdomyolysis; discontinue if unexplained muscle pain or weakness occurs.
Niacor (niacin) can cause profound flushing, which may be mitigated by taking aspirin 30 minutes prior or using extended-release formulations. Monitor liver function and blood glucose, as niacin can elevate transaminases and worsen glycemic control. Patients with gout may experience increased uric acid levels.
Take with meals to improve absorption and reduce gastrointestinal side effects.,Report unexplained muscle pain, tenderness, or weakness immediately, especially if also taking a statin.,Avoid alcohol consumption as it can worsen triglyceride levels and liver function.,You may need regular blood tests to monitor kidney function, liver enzymes, and lipid levels.,Do not take if you have severe kidney disease or active liver disease.
Take with food to reduce stomach upset.,Do not crush or chew extended-release tablets.,Flushing is common and may decrease with continued use.,Avoid alcohol and hot beverages near dosing time to reduce flushing.,Report unexplained muscle pain, tenderness, or weakness.,Monitor blood sugar if diabetic.,Do not substitute with dietary supplements without doctor approval.
No interactions on record
No interactions on record
Explore head-to-head clinical comparisons of other medications in the same therapeutic classes.
Common clinical questions about TRIGLIDE vs NIACOR, answered by our medical review team.
TRIGLIDE is a Fibrate Antilipemic that works by TRIGLIDE (fenofibrate) is a peroxisome proliferator-activated receptor alpha (PPARα) activator. It increases lipolysis and elimination of triglyceride-rich particles from plasma by activating lipoprotein lipase and reducing production of apolipoprotein C-III.. NIACOR is a Antilipemic agent that works by Niacin (nicotinic acid) reduces VLDL and LDL synthesis by inhibiting lipolysis in adipose tissue, decreasing free fatty acid flux to the liver, and inhibiting hepatic triglyceride synthesis. It also increases HDL by reducing catabolism of apolipoprotein A-I.. They differ in pharmacokinetic profiles, FDA-approved indications, and side effect profiles.
Potency comparisons between TRIGLIDE and NIACOR depend on the specific clinical indication. These are agents from distinct pharmacological classes and are not directly interchangeable by dose. A physician or clinical pharmacist should guide any therapeutic switching decisions.
The standard adult dose of TRIGLIDE is: Initial dose: 60 mg (1 tablet) twice daily, gradually increased over 3-7 days to maintenance dose of 120 mg twice daily.. The standard adult dose of NIACOR is: Initial: 250 mg orally once daily after evening meal; titrate up by 250–500 mg/day every 2–4 weeks. Maintenance: 1–2 g/day in divided doses (2–3 times daily). Maximum: 6 g/day.. Dosing should always be individualized based on indication, renal and hepatic function, age, and other patient factors.
No direct drug-drug interaction has been formally documented between TRIGLIDE and NIACOR in current clinical databases. However, individual patient risk factors including other medications, organ function, and comorbidities should always be evaluated by a qualified healthcare provider.
The maternal-fetal safety profiles differ. TRIGLIDE is classified as Category C. TRIGLIDE (fenofibrate) is contraindicated in pregnancy due to potential fetal harm. First trimester: no adequate human data; animal studies show embryotoxicity and delayed ossifica. NIACOR is classified as Category C. FDA Pregnancy Category C. Niacin is not recommended for use in pregnant women due to potential fetal harm, though no well-controlled studies exist. In animal studies, high doses ha. Always consult a maternal-fetal medicine specialist before taking either drug during pregnancy or lactation.