A Comprehensive Monograph on Fenofibric Acid (DB13873): Pharmacology, Clinical Efficacy, and Safety Profile

Executive Summary

Fenofibric acid (DrugBank ID: DB13873) is the pharmacologically active metabolite of the prodrug fenofibrate and a member of the fibric acid derivative (fibrate) class of antilipemic agents.[1] As a small molecule, it plays a critical role in the management of dyslipidemia, particularly conditions characterized by elevated triglycerides. The primary mechanism of action of fenofibric acid is its function as a potent agonist of the Peroxisome Proliferator-Activated Receptor alpha (PPARα).[1] Activation of this nuclear receptor modulates the transcription of a cascade of genes integral to lipid and lipoprotein metabolism. This results in a comprehensive improvement of the lipid profile, characterized by a substantial reduction in triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), total cholesterol (TC), and apolipoprotein B (Apo B), coupled with a clinically significant increase in high-density lipoprotein cholesterol (HDL-C).[1]

The principal therapeutic indications for fenofibric acid include severe hypertriglyceridemia (where it is used to reduce the risk of pancreatitis), primary hypercholesterolemia, and mixed dyslipidemia.[1] Its development was driven by the need to overcome the pharmacokinetic limitations of its parent compound, fenofibrate, such as poor bioavailability and a pronounced food effect. Formulations of fenofibric acid, such as choline fenofibrate (Trilipix) and fenofibric acid tablets (Fibricor), offer improved and more consistent absorption.[1] A landmark in its regulatory history is its approval by the U.S. Food and Drug Administration (FDA) for co-administration with HMG-CoA reductase inhibitors (statins), a distinction that sets it apart from other fibrates and positions it as a key agent for managing residual cardiovascular risk in patients with atherogenic dyslipidemia.[9]

The pharmacokinetic profile of fenofibric acid is favorable for clinical use. It is highly protein-bound (~99%), is primarily metabolized via glucuronidation independent of the cytochrome P450 enzyme system, and possesses an elimination half-life of approximately 20 hours, which supports a convenient once-daily dosing schedule.[5] This metabolic pathway minimizes the potential for significant pharmacokinetic drug-drug interactions with statins, a critical safety advantage.

The safety profile of fenofibric acid is well-characterized. Common adverse events include abnormal liver function tests, gastrointestinal disturbances, and rhinitis.[12] More serious, albeit less common, risks include myopathy and rhabdomyolysis, particularly when used in combination with statins, as well as hepatotoxicity, pancreatitis, and cholelithiasis.[12] Consequently, the drug is contraindicated in patients with severe renal impairment, active liver disease, or pre-existing gallbladder disease.[14] Effective risk management requires careful patient selection and periodic monitoring of liver function, renal function, and creatine phosphokinase (CPK) levels. In summary, fenofibric acid is an essential therapeutic option for managing complex lipid disorders, offering a targeted mechanism to address the triglyceride and HDL-C components of atherogenic dyslipidemia that are often inadequately controlled by statin monotherapy.

Drug Profile and Development

This section establishes the fundamental chemical identity of fenofibric acid and traces its regulatory and commercial trajectory, contextualizing its place in the therapeutic landscape.

Chemical and Physical Properties

Fenofibric acid is the active pharmacological entity responsible for the lipid-modifying effects of the widely prescribed drug fenofibrate.[1] Chemically, it is a monocarboxylic acid classified as a chlorobenzophenone and an aromatic ketone. Its systematic IUPAC name is 2-[4-(4-chlorobenzoyl)phenoxy]-2-methylpropanoic acid, which precisely describes its structure: a 2-methylpropanoic acid core substituted at the second carbon position with a 4-(4-chlorobenzoyl)phenoxy group.[1]

The molecular formula of fenofibric acid is C17​H15​ClO4​, corresponding to a molecular weight of 318.75 g/mol.[2] At ambient conditions, it presents as a white to almost white crystalline powder or solid.[2] The melting point of the compound is consistently reported within a narrow range of 179.0 °C to 183.0 °C, indicative of its high purity in pharmaceutical preparations.[16]

A cornerstone of modern drug development and regulation is the precise identification of a chemical entity across various databases and systems. The development of fenofibric acid formulations was a direct and strategic response to the clinical limitations of its prodrug, fenofibrate. Early formulations of fenofibrate were highly lipophilic and virtually insoluble in water, leading to poor and variable gastrointestinal absorption that was heavily dependent on the fat content of meals.[1] This food effect, which could increase bioavailability by as much as 35%, introduced a significant degree of therapeutic unpredictability and posed a challenge to patient compliance.[19] By formulating the active metabolite, fenofibric acid, directly—for instance, as a choline salt in Trilipix or as tablets in Fibricor—pharmaceutical scientists were able to engineer products with superior pharmacokinetic profiles.[1] These newer formulations exhibit improved bioavailability and can be administered without regard to meals, ensuring more consistent plasma concentrations and a more predictable clinical response, thereby representing a significant therapeutic optimization over the parent compound.[7]

Table 1: Chemical and Physical Identifiers of Fenofibric Acid

Property	Value	Source(s)
IUPAC Name	2-[4-(4-chlorobenzoyl)phenoxy]-2-methylpropanoic acid	1
CAS Number	42017-89-0	1
DrugBank ID	DB13873	1
Molecular Formula	C17​H15​ClO4​	6
Molecular Weight	318.75 g/mol	2
Physical Appearance	White to off-white crystalline powder/solid	2
Melting Point	179.0 - 183.0 °C	16
Synonyms	Procetofenic Acid, FNF Acid, NSC 281318	1
InChI	InChI=1S/C17H15ClO4/c1-17(2,16(20)21)22-14-9-5-12(6-10-14)15(19)11-3-7-13(18)8-4-11/h3-10H,1-2H3,(H,20,21)	1
InChIKey	MQOBSOSZFYZQOK-UHFFFAOYSA-N	1
SMILES	CC(C)(C(=O)O)OC1=CC=C(C=C1)C(=O)C2=CC=C(C=C2)Cl	1

Regulatory and Commercial Status

The regulatory journey of fenofibric acid in the United States is marked by key approvals that established its role in dyslipidemia management. The brand name Trilipix, a delayed-release capsule formulation of choline fenofibrate that delivers fenofibric acid as its active moiety, received its initial FDA approval on December 15, 2008, with AbbVie Inc. as the sponsoring company.[9] This was followed by the approval of Fibricor, a tablet formulation of fenofibric acid, on August 14, 2009, for Mutual Pharmaceutical Company, Inc..[25]

A pivotal moment in the drug's history, and a significant differentiator in the fibrate class, was the FDA's approval of Trilipix for use in combination with a statin.[9] This was the first and only such indication granted to a fibrate, specifically for the purpose of reducing triglycerides and increasing HDL-C in patients with mixed dyslipidemia and established coronary heart disease (CHD) or a CHD risk equivalent who were already on optimal statin therapy to manage their LDL-C.[26] This specific approval directly addressed a prevalent clinical challenge: the management of residual cardiovascular risk driven by atherogenic dyslipidemia. For years, clinicians had been hesitant to combine fibrates with statins due to a well-documented increased risk of myopathy and rhabdomyolysis, a concern largely driven by data from studies involving gemfibrozil.[3] The pharmacokinetic profile of fenofibric acid, which lacks significant interaction with the metabolic pathways of most statins, provided a stronger safety rationale for its combined use.[28] By pursuing and securing this specific indication, the manufacturer provided a regulatory assurance of safety and efficacy that distinguished Trilipix from other fibrates, including generic fenofibrate. This strategic regulatory achievement not only created a powerful marketing advantage but also influenced clinical practice by providing a clear, FDA-sanctioned option for treating a high-risk patient population.

The commercial landscape for fenofibric acid has since evolved with the introduction of generic alternatives. Mylan Pharmaceuticals Inc. launched one of the first generic versions of Trilipix, Fenofibric Acid Delayed-release Capsules in 45 mg and 135 mg strengths, on July 15, 2013, after receiving final approval for its Abbreviated New Drug Application (ANDA).[29] At the time of its generic launch, the brand product had annual U.S. sales of approximately $553.6 million, indicating a substantial market.[29]

Fenofibric acid is a component of the larger global fibrate drugs market, which was valued at $3.49 billion in 2024 and is projected to reach $4.72 billion by 2029, with a compound annual growth rate (CAGR) of 7.2%.[30] This growth is largely driven by the increasing global prevalence of cardiovascular diseases and metabolic disorders.[30] Within this market, the fenofibric acids sub-segment includes both capsule and combination product formulations.[32] North America currently represents the largest regional market for fibrate drugs, reflecting high rates of dyslipidemia and advanced healthcare infrastructure.[30] Key corporate players in the manufacturing and marketing of fenofibric acid include AbbVie, Mylan, Lupin, and Par Pharmaceutical.[34]

Clinical Pharmacology

This section provides a detailed analysis of the molecular mechanisms through which fenofibric acid exerts its therapeutic effects and describes its absorption, distribution, metabolism, and excretion within the human body.

Mechanism of Action (Pharmacodynamics)

The therapeutic effects of fenofibric acid are mediated primarily through its activity as an agonist for the Peroxisome Proliferator-Activated Receptor alpha (PPARα).[1] PPARα is a ligand-activated nuclear transcription factor that plays a central role in regulating the expression of genes involved in fatty acid and lipoprotein metabolism, glucose homeostasis, and inflammation.[4] Upon binding, fenofibric acid induces a conformational change in the PPARα receptor, which then heterodimerizes with the retinoid X receptor (RXR). This complex binds to specific DNA sequences known as peroxisome proliferator response elements (PPREs) in the promoter regions of target genes, thereby modulating their transcription.[4]

The downstream effects of PPARα activation are multifaceted and comprehensively address the key features of atherogenic dyslipidemia:

• Triglyceride Metabolism: Fenofibric acid profoundly reduces plasma triglyceride levels through several coordinated actions. First, it significantly upregulates the gene expression and synthesis of lipoprotein lipase (LPL), the rate-limiting enzyme for the hydrolysis of triglycerides within triglyceride-rich lipoproteins such as very-low-density lipoproteins (VLDL) and chylomicrons.[5] Second, it concurrently downregulates the expression of apolipoprotein C-III (ApoC-III), a potent inhibitor of LPL activity.[4] The dual effect of increasing LPL and decreasing its primary inhibitor leads to a marked acceleration of the catabolism and clearance of triglyceride-rich particles from the circulation. Third, PPARα activation enhances hepatic fatty acid uptake and stimulates mitochondrial β-oxidation by increasing the expression of key enzymes like acyl-CoA synthetase, thereby shunting fatty acids toward energy production and away from triglyceride synthesis and VLDL assembly.[4]
• HDL Metabolism: Fenofibric acid effectively raises HDL-C levels by stimulating the transcription of the genes encoding for apolipoprotein A-I (ApoA-I) and apolipoprotein A-II (ApoA-II), the principal structural proteins of HDL particles.[4] This increased synthesis of apolipoproteins promotes the formation of new HDL particles. Further research has elucidated a more intricate mechanism involving the ATP-binding cassette transporter A1 (ABCA1), which is critical for the efflux of cholesterol from peripheral cells to lipid-poor ApoA-I, the first step in reverse cholesterol transport. Fenofibric acid has been shown to enhance the transcription of the ABCA1 gene in a Liver X Receptor (LXR)-dependent manner, providing an additional pathway through which it promotes HDL biogenesis.[35]
• LDL Metabolism: The impact of fenofibric acid on LDL-C is more complex than that of statins. While it can produce a modest reduction in LDL-C concentrations (15-20%), its more clinically significant effect is on the qualitative characteristics of LDL particles.[19] In states of hypertriglyceridemia, the LDL profile is often dominated by small, dense LDL (sdLDL) particles, which are considered highly atherogenic due to their increased susceptibility to oxidation and prolonged residence time in circulation. By reducing the pool of triglyceride-rich VLDL particles, fenofibric acid indirectly promotes a shift in LDL particle distribution from these pathogenic sdLDL particles toward larger, more buoyant LDL particles. These larger particles have a higher affinity for the LDL receptor and are cleared more rapidly from the plasma, resulting in a less atherogenic overall lipoprotein profile.[19]

Beyond its primary role as a lipid modulator via PPARα, fenofibric acid exhibits a range of other pharmacological activities that may contribute to its overall clinical effects. These pleiotropic actions suggest that its benefits could extend beyond simple lipid correction. For instance, in vitro assays show that fenofibric acid also functions as an agonist for PPARγ and PPARδ, though with lower potency than for PPARα.[21] As PPARγ is the molecular target for thiazolidinedione drugs used in diabetes, this activity could contribute to effects on insulin sensitivity. Furthermore, fenofibric acid demonstrates direct anti-inflammatory properties by inhibiting cyclooxygenase-2 (COX-2) activity, an effect observed both in cell-free assays and in vivo animal models of inflammation.[21] This anti-inflammatory action may be a key contributor to its observed microvascular benefits and its potential to stabilize atherosclerotic plaques. Additionally, fenofibric acid has a well-documented uricosuric effect, reducing serum uric acid levels by increasing its renal excretion, which provides an ancillary benefit for patients with comorbid hyperuricemia or gout.[5] This combination of potent lipid modification, anti-inflammatory activity, and metabolic effects positions fenofibric acid as a comprehensive agent for managing the multifaceted nature of cardiometabolic disease.

Pharmacokinetics (Absorption, Distribution, Metabolism, and Excretion - ADME)

The pharmacokinetic profile of fenofibric acid is central to its clinical utility, particularly in comparison to its prodrug, fenofibrate.

• Absorption: Fenofibric acid is the active moiety of fenofibrate. When fenofibrate is administered orally, it is a prodrug that must be rapidly and completely hydrolyzed by tissue and plasma esterases (primarily carboxylesterase 1 in the liver) to fenofibric acid to become active.[7] The absorption of fenofibrate itself is limited by its poor water solubility and is significantly enhanced by the presence of food, which increases its bioavailability by approximately 35%.[17] This food-dependent absorption can lead to variability in drug exposure. To address this, formulations containing fenofibric acid itself (e.g., Fibricor) or a salt form that rapidly dissociates to fenofibric acid (e.g., choline fenofibrate in Trilipix) were developed. These formulations exhibit improved bioavailability and can be administered without regard to meals, providing more consistent absorption and predictable therapeutic effects.[7] After administration, peak plasma concentrations ( Tmax​) of fenofibric acid are typically reached within 4 to 8 hours, though this can vary depending on the specific formulation and the presence of food.[19]
• Distribution: Following absorption, fenofibric acid is extensively bound to plasma proteins, with approximately 99% bound to albumin.[5] This high degree of protein binding is consistent across both healthy and hyperlipidemic individuals. The apparent volume of distribution ( Vd​) is approximately 0.89 L/kg, suggesting distribution primarily within the vascular and well-perfused compartments.[11] With once-daily dosing, steady-state plasma concentrations of fenofibric acid are achieved within 5 to 9 days.[5]
• Metabolism: A key feature of fenofibric acid's pharmacology is its metabolic pathway, which is largely independent of the cytochrome P450 (CYP) enzyme system.[12] This characteristic is fundamental to its relatively favorable drug-drug interaction profile, particularly when co-administered with statins. Many statins, such as atorvastatin and simvastatin, are substrates for CYP3A4, and their metabolism can be inhibited by other drugs, leading to increased systemic exposure and a heightened risk of myopathy. In contrast, fenofibric acid does not undergo significant oxidative metabolism. Its primary metabolic fate is phase II conjugation with glucuronic acid, a reaction primarily catalyzed by the UDP-glucuronosyltransferase (UGT) isoform UGT1A9.[5] A minor metabolic route involves the reduction of the carbonyl moiety to a benzhydrol metabolite, which is subsequently also glucuronidated before excretion.[11] This lack of reliance on the CYP system means fenofibric acid does not compete for the same metabolic enzymes as many statins, providing a pharmacokinetic basis for its safer use in combination therapy compared to other fibrates like gemfibrozil, which is a known inhibitor of statin metabolism.[28]
• Excretion: Fenofibric acid and its metabolites are eliminated predominantly by the kidneys. Approximately 60% of an administered dose is recovered in the urine, primarily in the form of fenofibric acid glucuronide.[5] Around 25% of the dose is excreted in the feces.[5] The elimination half-life ( t1/2​) of fenofibric acid is approximately 20 to 23 hours, a duration that is sufficiently long to support a convenient once-daily dosing regimen.[5]

Table 2: Summary of Key Pharmacokinetic Parameters of Fenofibric Acid

Parameter	Value / Description	Source(s)
Bioavailability	Improved in fenofibric acid formulations; can be taken without regard to meals. Fenofibrate (prodrug) absorption increases ~35% with food.	8
Time to Peak (Tmax​)	4 - 8 hours (variable by formulation)	19
Protein Binding	~99% (primarily to albumin)	5
Volume of Distribution (Vd​)	~0.89 L/kg	11
Primary Metabolism	Glucuronidation (via UGT1A9); not significantly metabolized by CYP450 enzymes.	11
Elimination Half-Life (t1/2​)	~20 - 23 hours	5
Route of Excretion	~60% renal (urine); ~25% fecal	5

Clinical Efficacy and Therapeutic Applications

This section critically evaluates the clinical evidence supporting the use of fenofibric acid across its approved indications, analyzes its role in cardiovascular risk reduction based on major outcome trials, and explores its potential in other areas of medicine.

Management of Severe Hypertriglyceridemia (TG ≥ 500 mg/dL)

Fenofibric acid is a cornerstone of therapy for severe hypertriglyceridemia, defined as fasting triglyceride levels of 500 mg/dL or higher.[26] In this clinical setting, the immediate therapeutic objective extends beyond cardiovascular risk reduction to the prevention of acute pancreatitis, a serious and potentially life-threatening complication of markedly elevated triglycerides (e.g., >2000 mg/dL).[26]

Fenofibric acid, along with its parent compound fenofibrate, is considered a first-line pharmacologic treatment for this condition.[1] Clinical data consistently demonstrate its potent triglyceride-lowering efficacy, with studies showing reductions of up to 50-60% from baseline.[1] This robust effect is a direct consequence of its PPARα-mediated mechanism, which enhances the catabolism of triglyceride-rich lipoproteins.

It is critical to emphasize that pharmacotherapy is an adjunct to, not a replacement for, intensive lifestyle modification. The management of severe hypertriglyceridemia requires a comprehensive approach that includes a very low-fat diet (often restricting fat to <10% of total calories), complete abstinence from alcohol, and rigorous management of secondary factors that can exacerbate hypertriglyceridemia, such as poorly controlled diabetes mellitus and hypothyroidism.[1]

Management of Primary Hypercholesterolemia and Mixed Dyslipidemia

Fenofibric acid is also approved for the management of primary hypercholesterolemia and mixed dyslipidemia, conditions characterized by elevations in LDL-C, total cholesterol, and triglycerides, often accompanied by low levels of HDL-C.[1] While statins are the primary therapy for lowering LDL-C, fenofibric acid offers a complementary mechanism that is particularly effective for addressing the triglyceride and HDL components of dyslipidemia.

In the context of mixed dyslipidemia, fenofibric acid is most valuable as part of a combination therapy regimen with a statin. This approach targets multiple lipid abnormalities simultaneously. The efficacy of this strategy has been validated in several Phase 3 clinical trials.[47] For example, a large, randomized, double-blind study evaluated the combination of fenofibric acid (135 mg, referred to as ABT-335 in the trial) with rosuvastatin in patients with mixed dyslipidemia.[48] The results were compelling: compared to rosuvastatin 10 mg monotherapy, the combination with fenofibric acid produced significantly greater improvements in both HDL-C (a 20.3% increase vs. 8.5% for rosuvastatin alone) and triglycerides (a 47.1% reduction vs. 24.4% for rosuvastatin alone). The combination also led to a more substantial reduction in LDL-C (-37.2%) than fenofibric acid monotherapy (-6.5%).[48]

Similarly, a pooled analysis of three large trials focusing on 1,393 women with mixed dyslipidemia found that combination therapy with fenofibric acid and a low- or moderate-dose statin was superior to statin monotherapy in improving non-LDL parameters.[49] The moderate-dose combination therapy increased HDL-C by 21% and decreased triglycerides by 44%, compared to an 8% increase and a 26% decrease, respectively, with moderate-dose statin alone. Notably, the overall lipid profile achieved with this combination therapy was comparable or superior to that achieved with high-dose statin monotherapy, but with the potential for better tolerability.[49]

Table 3: Summary of Efficacy in Hypertriglyceridemia and Mixed Dyslipidemia Trials

Trial / Study	Patient Population	Treatment Arms	Baseline TG (mg/dL)	Baseline HDL-C (mg/dL)	% Change TG	% Change HDL-C	% Change LDL-C	Source(s)
Severe Hypertriglyceridemia (General Efficacy)	Patients with severe HTG (≥500 mg/dL)	Fenofibrate/Fenofibric Acid	>500	N/A	↓ up to 60%	↑ 10-20%	↓ 15-20%	1
Phase 3 Combination Trial (Rosuvastatin)	Patients with mixed dyslipidemia	Fenofibric Acid 135 mg + Rosuvastatin 10 mg	≥150	<40 (men) <50 (women)	↓ 47.1%	↑ 20.3%	↓ 37.2%	48
Phase 3 Combination Trial (Rosuvastatin)	Patients with mixed dyslipidemia	Rosuvastatin 10 mg monotherapy	≥150	<40 (men) <50 (women)	↓ 24.4%	↑ 8.5%	N/A	48
Pooled Analysis in Women	Women with mixed dyslipidemia	Fenofibric Acid + Moderate-Dose Statin	≥150	<50	↓ 44%	↑ 21%	↓ 37-39%	49
Pooled Analysis in Women	Women with mixed dyslipidemia	Moderate-Dose Statin monotherapy	≥150	<50	↓ 26%	↑ 8%	↓ 36-43%	49

Analysis of Major Cardiovascular Outcome Trials (ACCORD & FIELD)

The role of fenofibrate in reducing the risk of major cardiovascular events has been scrutinized in two landmark clinical trials: the ACCORD (Action to Control Cardiovascular Risk in Diabetes) Lipid trial and the FIELD (Fenofibrate Intervention and Event Lowering in Diabetes) study. Both trials enrolled thousands of patients with type 2 diabetes mellitus. The top-line results of both studies were neutral; neither demonstrated a statistically significant reduction in its primary composite cardiovascular endpoint when fenofibrate was compared to placebo (in FIELD) or added to simvastatin therapy (in ACCORD).[3]

However, a deeper analysis of these trials reveals a more nuanced and clinically important story. The failure to show a universal benefit should not be misinterpreted as a failure of the drug itself, but rather as a reflection of improper patient targeting in the overall trial populations. The primary mechanism of fenofibric acid is to correct abnormalities in triglycerides and HDL-C. It is therefore logical that its cardiovascular benefits would be most apparent in patients for whom these lipid abnormalities are the principal drivers of residual risk.

This hypothesis is strongly supported by pre-specified subgroup analyses from both trials. In a subgroup of patients with "atherogenic dyslipidemia"—defined by high baseline triglycerides (≥204 mg/dL) and low HDL-C (≤34 mg/dL)—the addition of fenofibrate resulted in a significant relative risk reduction in cardiovascular events.[1] This consistent finding across two large, independent trials provides compelling evidence that fenofibric acid therapy is effective in a specific, high-risk metabolic phenotype that is not fully addressed by statin therapy alone. This has led to a paradigm shift in clinical practice, moving away from the broad application of fibrates toward a more personalized approach, reserving their use for patients with this specific lipid profile.

Furthermore, the FIELD trial uncovered significant microvascular benefits associated with fenofibrate therapy, independent of its effects on major atherosclerotic events.[17] Patients treated with fenofibrate experienced a significant reduction in the progression of diabetic retinopathy and a decreased need for laser photocoagulation therapy. The trial also reported a 37% reduction in the risk of non-traumatic amputations below the ankle.[17] These findings are profound, as they suggest that the therapeutic effects of fenofibric acid extend beyond the modification of large-vessel atherosclerosis. These microvascular benefits are likely mediated by the drug's pleiotropic effects, such as its anti-inflammatory properties and its ability to improve endothelial function. This provides a distinct rationale for considering fenofibric acid in patients with diabetes, not only for lipid management but also for the prevention of debilitating microvascular complications.

Investigational and Off-Label Applications

The pharmacological profile of fenofibric acid has prompted research into its potential utility beyond dyslipidemia. A completed Phase 2 clinical trial (NCT02158273) explored the use of fenofibric acid in the context of medication development for alcohol dependency, suggesting an investigation into its potential neuromodulatory or metabolic effects related to addiction pathways.[51] Additionally, given its role in regulating fatty acid metabolism in the liver, fenofibrate has been studied for its potential in treating non-alcoholic fatty liver disease (NAFLD). Preclinical studies in mouse models have shown that it can effectively ameliorate the development of NAFLD, and it continues to be investigated as a potential therapy for this increasingly common metabolic liver disease.[17]

Safety, Tolerability, and Risk Management

This section provides a comprehensive overview of the safety profile of fenofibric acid, detailing its adverse effects, contraindications, and significant drug interactions to guide safe and effective clinical use.

Adverse Events Profile

The safety and tolerability of fenofibric acid have been extensively evaluated in clinical trials. While generally well-tolerated, it is associated with a range of adverse events from mild to severe.

• Common Adverse Events: Data from double-blind, placebo-controlled trials of fenofibrate provide the most reliable incidence rates for common side effects. The most frequently reported adverse reactions that occurred more often than with placebo are related to liver function and gastrointestinal or respiratory systems.[12] Other commonly reported side effects include back pain, headache, nausea, constipation, and arthralgia.[12]

Table 4: Frequency of Common Adverse Events from Placebo-Controlled Trials

Adverse Event	Fenofibrate* (N=439)	Placebo (N=365)
Abnormal Liver Function Tests	7.5%	1.4%
Respiratory Disorder	6.2%	5.5%
Abdominal Pain	4.6%	4.4%
Increased AST	3.4%	0.5%
Back Pain	3.4%	2.5%
Headache	3.2%	2.7%
Increased ALT	3.0%	1.6%
Increased CPK	3.0%	1.4%
Rhinitis	2.3%	1.1%
Nausea	2.3%	1.9%
Constipation	2.1%	1.4%
*Fenofibrate dosage equivalent to 105 mg or 135 mg fenofibric acid.
Source: 12

• Serious Adverse Events:
• Hepatotoxicity: Serious, idiosyncratic drug-induced liver injury, including cases of hepatitis, cirrhosis, and events requiring liver transplantation or resulting in death, has been reported with fenofibrate therapy.[12] This necessitates periodic monitoring of liver function tests (ALT, AST, total bilirubin) at baseline and during treatment.[55]
• Pancreatitis: Cases of pancreatitis have been reported. This may occur as a failure of efficacy in patients with severe hypertriglyceridemia, as a direct drug effect, or secondary to biliary sludge or stone formation leading to common bile duct obstruction.[53]
• Cholelithiasis: Fenofibric acid increases cholesterol saturation in the bile, which elevates the risk of forming gallstones (cholelithiasis).[12] If cholelithiasis is suspected, gallbladder studies are indicated.
• Hypersensitivity Reactions: Both immediate and delayed hypersensitivity reactions have been observed. Acute reactions include anaphylaxis and angioedema. Delayed reactions include severe cutaneous adverse reactions (SCAR) such as Stevens-Johnson Syndrome (SJS), Toxic Epidermal Necrolysis (TEN), and Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS).[14]
• Venothromboembolic Disease: Postmarketing reports have identified cases of pulmonary embolism (PE) and deep vein thrombosis (DVT) in patients taking fenofibrate.[56]
• Hematologic Changes: Mild to moderate decreases in hemoglobin, hematocrit, and white blood cell counts have been observed. Rare cases of agranulocytosis and thrombocytopenia have been reported. Periodic monitoring of blood counts is recommended during the first 12 months of therapy.[5]
• Paradoxical HDL-C Decrease: An important and counterintuitive adverse event is the report of severe, paradoxical decreases in HDL-C levels, sometimes to as low as 2 mg/dL.[12] This phenomenon directly contradicts the drug's intended therapeutic effect of raising HDL-C. The mechanism is unknown, but the effect is reported to be rapid and sustained upon withdrawal of the drug. This highlights the necessity of monitoring the full lipid panel within the first few months of initiating therapy and discontinuing the drug if a severe HDL-C depression is observed.

Myopathy and Rhabdomyolysis

Myopathy, characterized by diffuse myalgias, muscle tenderness, or weakness, accompanied by marked elevations in creatine phosphokinase (CPK) levels, is a known class effect of fibrates.[3] In rare instances, myopathy can progress to rhabdomyolysis, a severe condition involving the breakdown of skeletal muscle that releases myoglobin into the bloodstream, potentially leading to acute renal failure.[45]

The risk of myopathy is significantly amplified when fenofibric acid is co-administered with a statin.[3] While the risk is present, it is considered to be lower with fenofibric acid compared to gemfibrozil, due to differing effects on statin metabolism.[1] The risk is further heightened in specific patient populations, including the elderly and individuals with underlying conditions such as diabetes mellitus, renal impairment, or hypothyroidism.[3]

Effective risk management is paramount. It involves careful patient selection and comprehensive counseling. Patients must be instructed to promptly report any signs of muscle toxicity, such as unexplained muscle pain, tenderness, or weakness.[59] Regular monitoring of CPK levels should be considered, particularly in symptomatic patients or those with risk factors. If myopathy is suspected or diagnosed, fenofibric acid therapy should be discontinued immediately.[3]

Contraindications and Precautions

The use of fenofibric acid is strictly contraindicated in several patient populations due to an unacceptable risk of serious adverse events:

• Absolute Contraindications:
• Patients with severe renal impairment, defined as an estimated glomerular filtration rate (eGFR) less than 30 mL/min/1.73m², including those requiring dialysis.[5]
• Patients with active liver disease, including primary biliary cirrhosis and those with unexplained persistent elevations in serum transaminases.[5]
• Patients with pre-existing gallbladder disease.[5]
• Patients with a known hypersensitivity to fenofibric acid, fenofibrate, or any excipients in the formulation.[14]
• Nursing mothers, due to the potential for serious adverse reactions in the infant.[5]

The safety profile of fenofibric acid mandates a proactive and continuous monitoring strategy. Its prescription is not a single event but the initiation of a therapeutic partnership that requires ongoing surveillance. Clinicians must perform baseline and periodic assessments of renal function (serum creatinine) and liver function (ALT, AST).[12] This structured follow-up is essential for the early detection of potential toxicity and is as critical to the drug's overall safety as its intrinsic pharmacological properties.

Clinically Significant Drug-Drug Interactions

Fenofibric acid can interact with several other medications, necessitating careful management to avoid adverse outcomes.

Table 5: Clinically Significant Drug-Drug Interactions and Management Strategies

Interacting Drug/Class	Potential Effect	Mechanism (if known)	Clinical Management Recommendation	Source(s)
Statins (HMG-CoA Reductase Inhibitors)	Increased risk of myopathy and rhabdomyolysis.	Additive pharmacodynamic effects on muscle tissue.	Use with caution. Consider a lower statin dose. Avoid combination unless benefit outweighs risk. Monitor for muscle symptoms and CPK.	58
Coumarin Anticoagulants (e.g., Warfarin)	Potentiation of anticoagulant effect, increased risk of bleeding.	Displacement of anticoagulant from plasma protein binding sites.	Reduce anticoagulant dose upon initiation of fenofibric acid. Monitor PT/INR frequently until stabilized, then at usual intervals.	5
Cyclosporine	Increased risk of nephrotoxicity.	Synergistic adverse effects on renal function.	Use with caution. Monitor renal function closely. Therapy modification may be required.	5
Bile Acid Sequestrants (e.g., Cholestyramine)	Decreased absorption of fenofibric acid.	Binding of fenofibric acid in the gastrointestinal tract.	Administer fenofibric acid at least 1 hour before or 4 to 6 hours after the sequestrant.	17
Colchicine	Increased risk of myopathy and rhabdomyolysis.	Additive muscle toxicity.	Use with caution and monitor for signs of myopathy.	3

Dosage, Administration, and Formulations

This section provides practical, clinically-oriented information on the available formulations of fenofibric acid and guidelines for its appropriate dosage and administration.

Commercial Formulations and Bioequivalence

In the United States, fenofibric acid is commercially available in two primary forms: delayed-release capsules sold under the brand name Trilipix, and tablets sold under the brand name Fibricor.[3]

• Trilipix (choline fenofibrate) delayed-release capsules are available in two strengths: 45 mg and 135 mg.[24]
• Fibricor (fenofibric acid) tablets are available in two strengths: 35 mg and 105 mg.[39]

It is crucial for healthcare providers to recognize that different formulations of fenofibrate and fenofibric acid are not interchangeable on a milligram-for-milligram basis.[3] The development of formulations like Trilipix and Fibricor was specifically intended to improve upon the pharmacokinetic limitations of older fenofibrate products, particularly the significant food effect. As a result, both Trilipix and Fibricor can be administered without regard to meals, which simplifies the dosing regimen and enhances patient adherence compared to formulations that must be taken with food.[38]

Dosing and Administration Guidelines

Adherence to proper dosing and administration guidelines is essential for maximizing efficacy and minimizing risks.

• General Considerations: Before initiating therapy with fenofibric acid, patients should be placed on an appropriate lipid-lowering diet, and this diet should be continued throughout the course of treatment.[3] Both capsules and tablets must be swallowed whole; they should not be opened, crushed, dissolved, or chewed, as this can alter the drug's release profile.[5]
• Dosing for Severe Hypertriglyceridemia:
• The initial dose ranges from 45 to 135 mg once daily for Trilipix capsules or 35 to 105 mg once daily for Fibricor tablets.[38]
• The dosage should be individualized based on the patient's response. Lipid levels should be reassessed at 4 to 8-week intervals to guide any necessary dose adjustments.[5]
• The maximum recommended daily dose is 135 mg for capsules or 105 mg for tablets.[38]
• Dosing for Primary Hypercholesterolemia or Mixed Dyslipidemia:
• The recommended dose is 135 mg once daily for Trilipix capsules or 105 mg once daily for Fibricor tablets.[38]
• Dose Adjustments in Specific Populations:
• Renal Impairment: Dosage adjustment is mandatory for patients with impaired renal function. In patients with mild to moderate renal impairment (eGFR 30–59 mL/min/1.73 m²), treatment must be initiated at the lowest available dose: 45 mg once daily for capsules or 35 mg once daily for tablets.[3] Any subsequent dose increase should only be considered after a thorough evaluation of the effects on both renal function and lipid levels at the initial dose. Fenofibric acid is contraindicated in patients with severe renal impairment (eGFR <30 mL/min/1.73 m²).[3]
• Geriatric Use: For elderly patients, dose selection should not be based on age alone but should be guided by the patient's renal function, following the recommendations for renal impairment.[26]
• Hepatic Impairment: Fenofibric acid has not been formally studied in patients with hepatic impairment and is contraindicated in patients with active liver disease.[14]

Synthesis and Clinical Perspective

This concluding section synthesizes the comprehensive data presented into a cohesive clinical narrative, offering an expert perspective on the role and strategic positioning of fenofibric acid in the contemporary management of dyslipidemia.

Integrated Risk-Benefit Assessment

The clinical utility of fenofibric acid is determined by a careful balance of its substantial therapeutic benefits against its well-defined safety risks. The primary benefit of the drug is its potent and reliable effect on the lipid profile, particularly its ability to dramatically reduce triglyceride levels by up to 60% and significantly increase HDL-C levels by up to 25%.[1] This makes it an invaluable tool in specific clinical scenarios. In patients with severe hypertriglyceridemia, the benefit of preventing potentially fatal acute pancreatitis is clear and compelling. In patients with atherogenic dyslipidemia on statin therapy, the benefit lies in addressing the residual cardiovascular risk associated with high triglycerides and low HDL-C, a risk component that statins alone may not adequately control.

These benefits must be weighed against the risks of myopathy/rhabdomyolysis (particularly in combination with statins), hepatotoxicity, and cholelithiasis.[12] While these risks are serious, they are generally manageable through appropriate patient selection and a diligent monitoring protocol. The contraindications are clear: the drug should be avoided in patients with severe renal or hepatic disease and those with gallbladder disease. For the appropriately selected patient—one with a clear indication and without contraindications—the evidence suggests that the therapeutic benefits of fenofibric acid outweigh the potential risks, provided that a robust clinical surveillance plan for liver, kidney, and muscle function is implemented and maintained.

Strategic Positioning in Dyslipidemia Management

In the modern algorithm for dyslipidemia management, fenofibric acid is a specialized, second-line agent rather than a universal first-line therapy. Statins remain the undisputed cornerstone for the primary and secondary prevention of atherosclerotic cardiovascular disease, owing to their profound LDL-C lowering effects and overwhelming evidence of morbidity and mortality reduction in broad patient populations.[17]

The strategic niche for fenofibric acid is clearly defined. It is a first-line agent only in the context of severe hypertriglyceridemia for pancreatitis risk reduction. Its more common and arguably more important role is in the management of moderate hypertriglyceridemia and mixed dyslipidemia, specifically as an add-on to statin therapy. The ideal candidate for combination therapy is the patient who, despite being on an optimal or maximally tolerated statin dose with a controlled LDL-C, continues to exhibit the high-risk phenotype of atherogenic dyslipidemia: elevated triglycerides and low HDL-C.

The development of fenofibric acid formulations and the landmark FDA approval for statin co-administration have solidified its position as the fibrate of choice for this purpose. Its favorable pharmacokinetic profile, particularly the lack of significant CYP450-mediated interactions, gives it a distinct safety advantage over older fibrates like gemfibrozil when used with statins.[28]

Ultimately, the clinical narrative of fenofibric acid has evolved from the disappointing top-line results of large outcome trials in unselected populations to a more sophisticated understanding of its value in targeted therapy. The future of its use lies not in broad application but in a personalized medicine approach, where it is precisely deployed to manage the specific metabolic abnormalities and residual risk profile of the patient with atherogenic dyslipidemia. In this role, it remains an essential and effective component of the comprehensive cardiometabolic armamentarium.

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