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Triglide
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Overview
What is Triglide?
Triglide (fenofibrate) Tablets, is a lipid regulating agent available as tablets for oral administration. Each tablet contains 160 mg of fenofibrate.
The chemical name for fenofibrate is 2-[4-(4-chlorobenzoyl) phenoxy] 2-methyl-propanoic acid, 1-methylethyl ester with the following structural formula:
The empirical formula is CHOCl and the molecular weight is 360.83; fenofibrate is insoluble in water. The melting point is 79° to 82°C. Fenofibrate is a white solid which is stable under ordinary conditions.
What should I talk to my health care provider before I take Triglide?
How should I use Triglide?
Triglide is indicated as adjunctive therapy to diet to reduce elevated low-density lipoprotein cholesterol (LDL-C), total cholesterol (Total-C), Triglycerides, and apolipoprotein B (Apo B), and to increase high-density lipoprotein cholesterol (HDL-C) in adult patients with primary hypercholesterolemia or mixed dyslipidemia.
The dose of Triglide is 160 mg once daily.
Patients should be placed on an appropriate lipid-lowering diet before receiving Triglide and should continue this diet during treatment with Triglide.
Lipid levels should be monitored periodically. Therapy should be withdrawn in patients who do not have an adequate response after two months of treatment.
Triglide tablets can be given without regard to meals. Patients should be advised to swallow Triglide tablets whole. Do not crush, break, dissolve, or chew tablets.
What interacts with Triglide?
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What are the warnings of Triglide?
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What are the precautions of Triglide?
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What are the side effects of Triglide?
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What should I look out for while using Triglide?
Triglide is contraindicated in:
What might happen if I take too much Triglide?
There is no specific treatment for overdose with Triglide. General supportive care of the patient is indicated, including monitoring of vital signs and observation of clinical status, should an overdose occur. Ifindicated, elimination of unabsorbed drug should be achieved by emesis or gastric lavage; usual precautions should be observed to maintain the airway. Because fenofibrate is highly bound to plasma proteins, hemodialysis should not be considered.
How should I store and handle Triglide?
Store at 20° to 25°C (68° to 77°F) [See USP Controlled Room Temperature].Dispense in a tight, light-resistant container as defined in the USP, with a child-resistant closure (as required). Store at 20° to 25°C (68° to 77°F) [See USP Controlled Room Temperature].Dispense in a tight, light-resistant container as defined in the USP, with a child-resistant closure (as required). The tablets are supplied as follows:Only dispense Triglide tablets in the original manufacturer bottle with the original desiccant cap. Do not repackage Triglide tablets into standard amber pharmacy vials.The tablets are supplied as follows:Only dispense Triglide tablets in the original manufacturer bottle with the original desiccant cap. Do not repackage Triglide tablets into standard amber pharmacy vials.
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Clinical Information
Chemical Structure
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Clinical Pharmacology
The active moiety of Triglide is fenofibric acid. The pharmacological effects of fenofibric acid in both animals and humans have been extensively studied through oral administration of fenofibrate.
The lipid-modifying effects of fenofibric acid seen in clinical practice have been explained in transgenic mice and
in human hepatocyte cultures by the activation of peroxisome proliferators activated receptor α (PPARα). Through this mechanism, fenofibrate increases lipolysis and elimination of triglyceride-rich particles from plasma by activating lipoprotein lipase and reducing production of apoprotein C-III (an inhibitor of lipoprotein lipase activity).
The resulting decrease in TG produces an alteration in the size and composition of LDL from small, dense particles (which are thought to be artherogenic due to their susceptibility to oxidation), to large buoyant particles. These larger particles have a greater affinity for cholesterol receptors and are catabolized rapidly. Activation of PPARα also induces an increase in the synthesis of apoproteins A-I, A-II and HDL-cholesterol.
Fenofibrate also reduces serum uric acid levels in hyperuricemic and normal individuals by increasing the urinary excretion of uric acid.
Non-Clinical Toxicology
Triglide is contraindicated in:
Aminosalicylic acid at a dosage of 12 grams in a rapidly available form has been reported to produce a 20 percent reduction in the acetylation of isoniazid, especially in patients who are rapid acetylators; INH serum levels, half lives and excretions in fast acetylators still remain half of the levels seen in slow acetylators with or without p-aminosalicylic acid. The effect is dose related and, while it has not been studied with the current delayed release preparation, the lower serum levels with this preparation will result in a reduced effect on the acetylation of INH.
Aminosalicylic acid has previously been reported to block the absorption of rifampin. A subsequent report has shown that this blockade was due to an excipient not included in PASER granules. Oral administration of a solution containing both aminosalicylic acid and rifampin showed full absorption of each product.
As a result of competition, Vitamin B absorption has been reduced 55% by 5 grams of aminosalicylic acid with clinically significant erythrocyte abnormalities developing after depletion; patients on therapy of more than one month should be considered for maintenance B.
A malabsorption syndrome can develop in patients on aminosalicylic acid but is usually not complete. The complete syndrome includes steatorrhea, an abnormal small bowel pattern on x-ray, villus atrophy, depressed cholesterol, reduced D-xylose and iron absorption. Triglyceride absorption always is normal.
In one literature report 8 hours after the last dosage of aminosalicylic acid at 2 gm qid serum digoxin levels were reduced 40% in two of ten patients but not changed in the remaining eight.
The effect of Triglide on coronary heart disease morbidity and mortality and non-cardiovascular mortality has not been established.
The Action to Control Cardiovascular Risk in Diabetes Lipid (ACCORD Lipid) trial was a randomized placebo-controlled study of 5518 patients with type 2 diabetes mellitus on background statin therapy treated with fenofibrate. The mean duration of follow-up was 4.7 years. Fenofibrate plus statin combination therapy showed a non-significant 8% relative risk reduction in the primary outcome of major adverse cardiovascular events (MACE), a composite of non-fatal myocardial infarction, non-fatal stroke, and cardiovascular disease death (hazard ratio [HR] 0.92, 95% CI 0.79-1.08) (p=0.32) as compared to statin monotherapy. In a gender subgroup analysis, the hazard ratio for MACE in men receiving combination therapy versus statin monotherapy was 0.82 (95% CI 0.69-0.99), and the hazard ratio for MACE in women receiving combination therapy versus statin monotherapy was 1.38 (95% CI 0.98-1.94) (interaction p=0.01). The clinical significance of this subgroup finding is unclear.
The Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) study was a 5-year randomized, placebo-controlled study of 9,795 patients with type 2 diabetes mellitus treated with fenofibrate. Fenofibrate demonstrated a non-significant 11% relative reduction in the primary outcome of coronary heart disease events (hazard ratio [HR] 0.89, 95% CI 0.75-1.05, p=0.16) and a significant 11% reduction in the secondary outcome of total cardiovascular disease events (HR 0.89 [0.80-0.99], p=0.04). There was a non-significant 11% (HR 1.11 [0.95, 1.29], p=0.18) and 19% (HR 1.19 [0.90, 1.57], p=0.22) increase in total and coronary heart disease mortality, respectively, with fenofibrate as compared to placebo.
Because of chemical, pharmacological, and clinical similarities between Triglide (fenofibrate tablets), clofibrate, and gemfibrozil, the adverse findings in 4 large randomized, placebo-controlled clinical studies with these other fibrate drugs may also apply to Triglide.
In the Coronary Drug Project, a large study of post myocardial infarction of patients treated for 5 years with clofibrate, there was no difference in mortality seen between the clofibrate group and the placebo group. There was however, a difference in the rate of cholelithiasis and cholecystitis requiring surgery between the two groups (3.0% vs. 1.8%).
In a study conducted by the World Health Organization (WHO), 5000 subjects without known coronary artery disease were treated with placebo or clofibrate for 5 years and followed for an additional one year. There was a statistically significant, higher age-adjusted all-cause mortality in the clofibrate group compared with the placebo group (5.70% vs. 3.96%, p=<0.01). Excess mortality was due to a 33% increase in non-cardiovascular causes, including malignancy, post-cholecystectomy complications, and pancreatitis. This appeared to confirm the higher risk of gallbladder disease seen in clofibrate-treated patients studied in the Coronary Drug Project.
The Helsinki Heart Study was a large (n=4,081) study of middle-aged men without a history of coronary artery disease. Subjects received either placebo or gemfibrozil for 5 years, with a 3.5 year open extension afterward. Total mortality was numerically higher in the gemfibrozil randomization group but did not achieve statistical significance (p=0.19, 95% confidence interval for relative risk G:P=0.91-1.64). Although cancer deaths trended higher in the gemfibrozil group (p=0.11), cancers (excluding basal cell carcinoma) were diagnosed with equal frequency in both study groups. Due to the limited size of the study, the relative risk of death from any cause was not shown to be different than that seen in the 9 year follow-up data from the WHO study (RR=1.29).
A secondary prevention component of the Helsinki Heart Study enrolled middle-aged men excluded from the primary prevention study because of known or suspected coronary heart disease. Subjects received gemfibrozil or placebo for 5 years. Although cardiac deaths trended higher in the gemfibrozil group, this was not statistically significant (hazard ratio 2.2, 95% confidence interval: 0.94-5.05).
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Reference
This information is obtained from the National Institute of Health's Standard Packaging Label drug database.
"https://dailymed.nlm.nih.gov/dailymed/"
While we update our database periodically, we cannot guarantee it is always updated to the latest version.
Clonazepam Description
Each single-scored tablet, for oral administration, contains 0.5 mg, 1 mg, or 2 mg Clonazepam, USP, a benzodiazepine. Each tablet also contains corn starch, lactose monohydrate, magnesium stearate, microcrystalline cellulose, and povidone. Clonazepam tablets USP 0.5 mg contain Yellow D&C No. 10 Aluminum Lake. Clonazepam tablets USP 1 mg contain Yellow D&C No. 10 Aluminum Lake, as well as FD&C Blue No. 1 Aluminum Lake.
Chemically, Clonazepam, USP is 5-(o-chlorophenyl)-1,3-dihydro-7-nitro-2H-1,4-benzodiazepin-2-one. It is a light yellow crystalline powder. It has the following structural formula:
C15H10ClN3O3 M.W. 315.72
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Interactions
Interactions
A total of 440 drugs (1549 brand and generic names) are known to interact with Imbruvica (ibrutinib).
228 major drug interactions (854 brand and generic names)
210 moderate drug interactions (691 brand and generic names)
2 minor drug interactions (4 brand and generic names)
Show all medications in the database that may interact with Imbruvica (ibrutinib).
