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Totalip: Full Drug Profile

Medically reviewed by Min Clinic Staff | Updated: January 2026

Totalip - General Information

Totalip (Lipitor) is a member of the drug class known as statins. It is used for lowering cholesterol. Totalip inhibits the rate-determining enzyme located in hepatic tissue that produces mevalonate, a small molecule used in the synthesis of cholesterol and other mevalonate derivatives. This lowers the amount of cholesterol produced which in turn lowers the total amount of LDL cholesterol. Totalip is a competitive inhibitor of HMG-CoA reductase.

 

Pharmacology of Totalip

Totalip, a selective, competitive HMG-CoA reductase inhibitor, is used to lower cholesterol and triglycerides in patients with hypercholesterolemia and mixed dyslipidemia and in the treatment of homozygous familial hypercholesterolemia. Totalip has a unique structure, long half-life, and hepatic selectivity, explaining its greater LDL-lowering potency compared to other HMG-CoA reductase inhibitors.

 

Totalip for patients

Lipitor is a HMG-CoA Reductase Inhibitor, also known as a statin. This class of treatments for high cholesterol is fairly new, and appears to work by blocking a liver enzyme which generates cholesterol. This medication appears to be the most effective in this class of drugs at lowering unhealthy LDL (low-density lipoprotein) cholesterol levels, in some cases up to 51%. It can be virtually as effective as an angioplasty in treating stable coronary artery disease. Currently, this drug is approved for use in patients with high cholesterol (hypercholesterolemia) due to high LDL levels, hereditary elevated fat levels (dysbetalipoproteinemia), familial high cholesterol, and to increase HDL (high-density lipoprotein) levels in patients with high cholesterol and those with both high cholesterol and high triglycerides (mixed dyslipidemia). Other accepted uses include the treatment of stable coronary artery diseas, preventing coronary heart disease, preventing clogged stents (tubes) placed in coronary arteries after surgery, preventing bone loss in type two diabetics, stabilizing lipid levels that have been altered by treatment with protease inhibitors. This treatment should be considered a last resort. The best way to lower cholesterol is through a program of healthy diet and exercise, and these should be maintained during treatment with Lipitor.

 

Totalip Interactions

The risk of myopathy during treatment with drugs of this class is increased with concurrent administration of cyclosporine, fibric acid derivatives, niacin (nicotinic acid), erythromycin, azole antifungals.

Antacid: When atorvastatin and MaaloxÒ TC suspension were coadministered, plasma concentrations of atorvastatin decreased approximately 35%. However, LDL-C reduction was not altered.

Antipyrine: Because atorvastatin does not affect the pharmacokinetics of antipyrine, interactions with other drugs metabolized via the same cytochrome isozymes are not expected.

Colestipol: Plasma concentrations of atorvastatin decreased approximately 25% when colestipol and atorvastatin were coadministered. However, LDL-C reduction was greater when atorvastatin and colestipol were coadministered than when either drug was given alone.

Cimetidine: Atorvastatin plasma concentrations and LDL-C reduction were not altered by coadministration of cimetidine.

Digoxin: When multiple doses of atorvastatin and digoxin were coadministered, steady-state plasma digoxin concentrations increased by approximately 20%. Patients taking digoxin should be monitored appropriately.

Erythromycin: In healthy individuals, plasma concentrations of atorvastatin increased approximately 40% with coadministration of atorvastatin and erythromycin, a known inhibitor of cytochrome P450 3A4.

Oral Contraceptives: Coadministration of atorvastatin and an oral contraceptive increased AUC values for norethindrone and ethinyl estradiol by approximately 30% and 20%. These increases should be considered when selecting an oral contraceptive for a woman taking atorvastatin.

Warfarin: Atorvastatin had no clinically significant effect on prothrombin time when administered to patients receiving chronic warfarin treatment.

Endocrine Function

HMG-CoA reductase inhibitors interfere with cholesterol synthesis and theoretically might blunt adrenal and/or gonadal steroid production. Clinical studies have shown that atorvastatin does not reduce basal plasma cortisol concentration or impair adrenal reserve. The effects of HMG-CoA reductase inhibitors on male fertility have not been studied in adequate numbers of patients. The effects, if any, on the pituitary-gonadal axis in premenopausal women are unknown. Caution should be exercised if an HMG-CoA reductase inhibitor is administered concomitantly with drugs that may decrease the levels or activity of endogenous steroid hormones, such as ketoconazole, spironolactone, and cimetidine.

CNS Toxicity

Brain hemorrhage was seen in a female dog treated for 3 months at 120 mg/kg/day. Brain hemorrhage and optic nerve vacuolation were seen in another female dog that was sacrificed in moribund condition after 11 weeks of escalating doses up to 280 mg/kg/day. The 120 mg/kg dose resulted in a systemic exposure approximately 16 times the human plasma area-under-the-curve (AUC, 0-24 hours) based on the maximum human dose of 80 mg/day. A single tonic convulsion was seen in each of 2 male dogs (one treated at 10 mg/kg/day and one at 120 mg/kg/day) in a 2-year study. No CNS lesions have been observed in mice after chronic treatment for up to 2 years at doses up to 400 mg/kg/day or in rats at doses up to 100 mg/kg/day. These doses were 6 to 11 times (mouse) and 8 to 16 times (rat) the human AUC (0-24) based on the maximum recommended human dose of 80 mg/day.

CNS vascular lesions, characterized by perivascular hemorrhages, edema, and mononuclear cell infiltration of perivascular spaces, have been observed in dogs treated with other members of this class. A chemically similar drug in this class produced optic nerve degeneration (Wallerian degeneration of retinogeniculate fibers) in clinically normal dogs in a dose-dependent fashion at a dose that produced plasma drug levels about 30 times higher than the mean drug level in humans taking the highest recommended dose.

 

Totalip Contraindications

Active liver disease or unexplained persistent elevations of serum transaminases.

Hypersensitivity to any component of this medication.

Pregnancy and Lactation

Atherosclerosis is a chronic process and discontinuation of lipid-lowering drugs during pregnancy should have little impact on the outcome of long-term therapy of primary hypercholesterolemia. Cholesterol and other products of cholesterol biosynthesis are essential components for fetal development (including synthesis of steroids and cell membranes). Since HMG-CoA reductase inhibitors decrease cholesterol synthesis and possibly the synthesis of other biologically active substances derived from cholesterol, they may cause fetal harm when administered to pregnant women. Therefore, HMG-CoA reductase inhibitors are contraindicated during pregnancy and in nursing mothers. ATORVASTATIN SHOULD BE ADMINISTERED TO WOMEN OF CHILDBEARING AGE ONLY WHEN SUCH PATIENTS ARE HIGHLY UNLIKELY TO CONCEIVE AND HAVE BEEN INFORMED OF THE POTENTIAL HAZARDS. If the patient becomes pregnant while taking this drug, therapy should be discontinued and the patient apprised of the potential hazard to the fetus.

 

Additional information about Totalip

Totalip Indication: For management as an adjunct to diet to reduce elevated total-C, LDL-C, apo B, and TG levels in patients with primary hypercholesterolemia and mixed dyslipidemia. Mechanism Of Action: Totalip selectively and competitively inhibits the hepatic enzyme hydroxymethylglutaryl-coenzyme A (HMG-CoA) reductase. As HMG-CoA reductase is responsible for converting HMG-CoA to mevalonate, this results in a decrease in mevalonate, a precursor of cholesterol, and a subsequent decrease in hepatic cholesterol levels and increase in uptake of LDL cholesterol. Drug Interactions: Amprenavir Amprenavir can possibly increase the statinAtazanavir Atazanavir increases the effect and toxicity of the statinBosentan Bosentan could decrease atorvastatinCarbamazepine Carbamazepine decreases the effect of the statinClarithromycin The macrolide possibly increases the statin toxicityCyclosporine Possible myopathy and rhabdomyolysisDelavirdine The NNRT inhibitor increases the effect and toxicity of the statinDiltiazem Diltiazem increases the effect and toxicity of atorvastatinEfavirenz The NNRT inhibitor increases the effect and toxicity of the statinErythromycin The macrolide possibly increases the statin toxicityFenofibrate Increased risk of myopathy/rhabdomyolysisFluconazole Increased risk of myopathy/rhabdomyolysisFosamprenavir Amprenavir can possibly increase the statin toxicityGemfibrozil Increased risk of myopathy/rhabdomyolysisImatinib Imatinib increases the effect and toxicity of atorvastatinIndinavir Indinavir increases the effect and toxicity of atorvastatinItraconazole Increased risk of myopathy/rhabdomyolysisJosamycin The macrolide possibly increases the statin toxicityKetoconazole Increased risk of myopathy/rhabdomyolysisNefazodone Nefazodone increases the effect and toxicity of the statin drugNelfinavir Nelfinavir increases the effect and toxicity of the statinNevirapine The NNRT inhibitor increases the effect and toxicity of the statinQuinupristin This combination presents an increased risk of toxicityRifabutin The rifamycin decreases the effect of the statin drugRifampin The rifamycin decreases the effect of the statin drugRitonavir Ritonavir increases the effect and toxicity of the statinSaquinavir Saquinavir increases the effect and toxicity of atorvastatinTacrolimus Tacrolimus increases the effect and toxicity of the statinTelithromycin Telithromycin may possibly increase statin toxicityVerapamil Verapamil increases the effect and toxicity of the statinBezafibrate Increased risk of myopathy/rhabdomyolysisColchicine Increased risk of rhadbomyolysis with this combination Food Interactions: Avoid drastic changes in dietary habit.Avoid alcohol.Avoid taking grapefruit or grapefruit juice throughout treatment.Grapefruit can significantly increase serum levels of this product.Take with low fat meal.Food may decrease maximum plasma levels and area under the curve, but this is inconsequential according to the manufacturer. Generic Name: Atorvastatin Synonyms: Atorvastatin calcium Drug Category: Anticholesteremic Agents; Hydroxymethylglutaryl-CoA Reductase Inhibitors Drug Type: Small Molecule; Approved Other Brand Names containing Atorvastatin: Cardyl; Lipitor; Sotis; Torvast; Tozalip; Xavator; Sortis; Torvacard; Totalip; Tulip; Xarator; Atorpic; Liprimar; Absorption: Atorvastatin is rapidly absorbed after oral administration. The absolute bioavailability of atorvastatin (parent drug) is approximately 14% and the systemic availability of HMG-CoA reductase inhibitory activity is approximately 30%. Toxicity (Overdose): Symptoms of overdose include rhabdomyolysis, eye hemorrhages, and liver problems. Protein Binding: 98% Biotransformation: Atorvastatin is extensively metabolized to ortho- and parahydroxylated derivatives and various beta-oxidation products. In vitro inhibition of HMG-CoA reductase by ortho- and parahydroxylated metabolites is equivalent to that of atorvastatin. Approximately 70% of circulating inhibitory activity for HMG-CoA reductase is attributed to active metabolites. Half Life: 14 hours Dosage Forms of Totalip: Tablet Oral Chemical IUPAC Name: (3R,5R)-7-[2-(4-fluorophenyl)-3-phenyl-4-(phenylcarbamoyl)-5-propan-2-ylpyrrol-1-yl]-3,5-dihydroxyheptanoic acid Chemical Formula: C33H35FN2O5 Atorvastatin on Wikipedia: https://en.wikipedia.org/wiki/Atorvastatin Organisms Affected: Humans and other mammals