This information is for research and educational purposes only. No medical recommendations. Products are not approved for human use. For health questions, consult a doctor.

Atorvastatin (Lipitor)

The most prescribed statin in the world - relevant because oral anabolics flatten HDL.

3 min read 7 sources

To the sources

Compound approved · since 1996

Summary

At a glance

Sources checked on 26 Oct 2026

Coronary events (ASCOT-LLA)

−36 %

10,305 people with high blood pressure and average cholesterol, against placebo, stopped after 3.3 years¹

Major cardiovascular events (CARDS)

−37 %

2,838 people with type 2 diabetes without high LDL, ended two years early²

Highest versus lowest study dose (TNT)

−22 %

10,001 people with stable coronary disease, median 4.9 years³

Half-life

~14 hours

inhibition of the enzyme lasts 20 to 30 hours through active metabolites⁵

Atorvastatin is a statin. It inhibits HMG-CoA reductase in the liver, the liver cells then pull more LDL out of the blood.⁷⁵
In ASCOT-LLA coronary events fell by 36 percent in people with high blood pressure and average cholesterol, in CARDS major cardiovascular events fell by 37 percent in type 2 diabetes. Both trials ended early.¹²
In TNT the highest study dose lowered mean LDL to 2.0 instead of 2.6 mmol/l and events by 22 percent, while liver values stayed raised more often (1.2 versus 0.2 percent).³
After stroke or TIA (SPARCL) there were fewer strokes but slightly more brain bleeds. Muscle complaints and interactions via CYP3A4 are the known risks.⁴⁵
According to ChEMBL atorvastatin has been approved since 1996. Everything here is the state of research, not a recommendation.⁷

Profile

Updated July 2026

How long does it stay in the body?

Share left after one dose, calculated with a half-life of ~14 hours

Half-life ~14 hours

After 28 hours: 25 %

Hour 14 · 50 %Hour 24, next dose · 30 %Hour 28 · 25 %Hour 42 · 12.5 %Hour 70 · 3.1 %

Simplified model without an absorption phase, half-life from the TPD lexicon.

Class

Statin

HMG-CoA reductase inhibitor

Use

Oral

once daily in the evening

Half-life

about 14 hours

active metabolites longer

Metabolism

Via CYP3A4

correspondingly prone to interactions

Monitoring

Lipid panel before starting and no earlier than 6 weeks

Contents 12 sections

At a glance
What is atorvastatin?
How it works
Use and dosing
What the research shows
Research status
Side effects
Storage
Related compounds
FAQ
Glossary
Sources

What is atorvastatin?

Atorvastatin is a statin. It inhibits HMG-CoA reductase, the rate-limiting enzyme of the body's own cholesterol production in the liver. Less own production means the liver cell puts more LDL receptors on its surface and thereby pulls more LDL out of the blood. The actual effect therefore comes from that second step, not directly from the inhibition.

In the context of this platform it matters because oral anabolics flatten HDL and drive LDL up at the same time. That shift is one of the best documented consequences of oral 17-alpha-alkylated compounds.

This information is for research and educational purposes only. No medical advice.

Comparison

Three paths to less LDL

Statins, bempedoic acid and ezetimibe act at different points, as stated in the TPD lexicon. Tap a card to open its entry.

Statin Atorvastatin (Lipitor) HMGCR

Statin Rosuvastatin (Crestor) HMGCR ATP citrate lyase inhibitor Bempedoic acid (Nexletol) ACLY Gut uptake inhibitor Ezetimibe (Ezetrol, Zetia) NPC1L1

Simplified: statins and bempedoic acid slow cholesterol production in the liver, ezetimibe its uptake in the gut. ⁷

How it works

The body's own cholesterol synthesis peaks at night, hence the recommendation to take it in the evening. With atorvastatin that point is less critical than with the short-acting older statins, because the half-life of around 14 hours plus active metabolites covers a good part of the day anyway.

For dosing there is the so-called rule of six: each doubling of the dose lowers LDL by a further six percent. Going from 10 to 20mg therefore adds little, going from 10 to 80mg adds up, but the side effect price rises faster than the benefit. That is why the high dose only makes sense with a correspondingly high starting value.

Where it acts

Where atorvastatin acted in studies

Tap a point or a card. Colour = HMG-CoA reductase, grey = observed in studies.

Liver

Inhibits cholesterol production, more LDL receptors on the liver cell⁷

HMGCR
Blood lipids

Mean LDL 2.0 instead of 2.6 mmol/l (TNT)³

Observed in trials
Heart

36 percent fewer coronary events against placebo (ASCOT-LLA)¹

Observed in trials
Brain

Fewer strokes, slightly more brain bleeds (SPARCL)⁴

Observed in trials
Muscle

Muscle pain 3.5 versus 3.1 percent, rarely muscle breakdown⁵

Observed in trials

Targets in the ChEMBL database⁷

Compound CHEMBL393220: one recorded mechanism, Inhibitor, direct binding.

HMG-CoA reductase

Gene: HMGCR
UniProt: P04035
ChEMBL: CHEMBL402
Action: Inhibitor, direct binding

Honeycomb cells of light blue glass, in the central cell a blue gear-shaped enzyme with blue molecule chains docking onto it, golden spheres in docking sites along the cell edges — Atorvastatin inhibits HMG-CoA reductase in the liver cell. Symbolic image.

Use and dosing

Dosing

Dosing, titration and syringe

Loading the dosing information …

Getting started and stepping up, drawn as a staircase
Units on the U-100 syringe for every step
How long one vial lasts

Tablets in a blister. Symbolic image.

What the research shows

ASCOT-LLA (Lancet 2003) was stopped after 3.3 instead of the planned 5 years because the advantage was too clear: in hypertensives with average or even below-average cholesterol, 10mg atorvastatin cut coronary events by 36 percent. The message was new, because what was treated was not a high value but a high risk.

CARDS (Lancet 2004) did the same in type 2 diabetes and was likewise stopped two years early, with 37 percent fewer cardiovascular events. TNT (NEJM 2005) compared 80mg against 10mg in stable coronary disease and found 22 percent fewer events on the high dose, though with more liver value abnormalities.

SPARCL (NEJM 2006) belongs here with a caveat: after stroke or TIA, 80mg atorvastatin cut the stroke rate by 16 percent, while slightly more haemorrhagic strokes occurred. The net effect was positive, the limitation belongs in the picture anyway.

Study results

What the trials measured

Interactive: switch tabs, tap points, show or hide arms. Arms are named relative to each other, no dosing advice.

Fewer events in four large trials¹²⁴³

Relative risk reduction of the primary outcome, values from the abstracts

ASCOT-LLA¹ Coronary events, against placebo

Atorvastatin -36%

CARDS² Major cardiovascular events, against placebo

Atorvastatin -37%

SPARCL⁴ Stroke after stroke or TIA, against placebo

Atorvastatin -16%

TNT³ Major cardiovascular events, highest versus lowest dose

Highest study dose -22%

Calculated from the hazard ratios (0.64, 0.63 as a rate, 0.84 and 0.78). The trials differ in groups and outcomes, the bars cannot be read directly against each other.

Share with a major cardiovascular event³

10,001 people with stable coronary disease, median 4.9 years

TNT trial³

Lowest study dose 10.9%

Highest study dose 8.7%

Mean LDL 2.0 mmol/l on the highest dose and 2.6 mmol/l on the lowest. Overall mortality did not differ.

Repeat stroke within 4.9 years⁴

4,731 people after stroke or TIA, highest study dose against placebo

SPARCL trial⁴

Placebo 13.1%

Highest study dose 11.2%

Fewer ischaemic strokes (218 versus 274) but more brain bleeds (55 versus 33). Mortality was the same (216 versus 211 deaths).

Close-up of a cut, translucent blood vessel with a yellowish layer of deposits on the inner wall — The large trials measured heart attacks and strokes, not just lab values. Symbolic image.

Research status

Where the research stands

Atorvastatin has been approved since 1996. On ClinicalTrials.gov 1,197 trials list atorvastatin among their interventions, often as a comparator. Shown are the registered large outcome trials from this entry, ASCOT-LLA is not listed there. As of 26 Oct 2026. ⁶

Preclinical Principle: inhibition of HMG-CoA reductase in the liver
Phase 1 no registered trial
Phase 2 no registered trial
Phase 3 no registered trial
Approval since 1996

Approved: ChEMBL lists atorvastatin with phase 4 as the highest phase and first approval in 1996.⁷

Show all 3 phase 4 trials on a timelineHide timeline 3 completed 0 running 3 with results

Phase 4

Bar: start to primary endpoint (planned for running trials). Green = completed, blue = progress until 26 Oct 2026.

Side effects

Muscle pain: the best known issue. Statins can cause muscle pain and in rare cases genuine muscle breakdown. Anyone training hard has elevated CK anyway, which makes telling them apart difficult. New, unfamiliar muscle pain on a statin needs checking, not training through.
Liver values: small rises are common and usually harmless, clear rises need checking.
Blood sugar: statins slightly raise the risk of new-onset diabetes. The cardiovascular benefit clearly outweighs it in the trials, but it is worth mentioning.
Digestive complaints: common in the first weeks, usually temporary.

Tolerability

Side effects compared with placebo

Out of 100 participants per group, how many had the event over a median of 53 weeks.

3 of 100 Placebo

4 of 100 Atorvastatin

Event	Placebo	Atorvastatin
Muscle pain⁵	3%	4%
Joint pain⁵	7%	7%
Diarrhoea⁵	6%	7%
Persistently raised liver values (TNT)³	0%	0%

Values from the US label (all doses combined) and the TNT abstract. Rarely, muscle breakdown (rhabdomyolysis) and a rise in blood sugar and HbA1c are described.⁵³

Storage

Store dry, at room temperature and protected from light. Keep out of reach of children.

Three white tablet bottles on a bright shelf next to a folded light blue towel — Dry, at room temperature and away from light. Symbolic image.

Level · Atorvastatin (Lipitor)

How the level builds up

One dose per day: each dose adds to what is left of the previous one.

Lexicon: Oral, once daily in the evening

Peak 1.44×Trough 0.44×

Day 2 · 3. dose
1.4× of the first dose

Plateau

from Day 2

97 % of the plateau after dose 3

Peak

1.44×

of the first dose

Trough

0.44×

before the next dose

Simplified model, values relative to the first dose, no dosing information. Dashed: the first dose alone, green: the plateau.

Related compounds

Same targets or a different path: all in the TPD lexicon.

Atorvastatin (Lipitor)

Rosuvastatin (Crestor) Another statin, hardly broken down via CYP3A4 Bempedoic acid (Nexletol) Slows cholesterol production one step earlier

Ezetimibe (Ezetrol, Zetia) Slows cholesterol uptake in the gut

Telmisartan Different path, blood pressure instead of blood lipids Metformin (Glucophage) Different path, blood sugar instead of blood lipids

FAQ

Common questions about Atorvastatin (Lipitor)

Short answers, each backed by the sources below.

How does atorvastatin lower LDL?

It inhibits HMG-CoA reductase, the key enzyme of cholesterol production in the liver. The liver cell then puts more LDL receptors on its surface and pulls more LDL out of the blood. The half-life is about 14 hours, inhibition of the enzyme lasts 20 to 30 hours through active metabolites.⁷⁵

Is atorvastatin approved?

Yes. ChEMBL lists atorvastatin as an approved compound with first approval in 1996. On ClinicalTrials.gov 1,197 trials list atorvastatin among their interventions (as of 26 October 2026). Everything here is the state of research, not a recommendation.⁷⁶

What did ASCOT-LLA and CARDS show?

Both tested people without notably high cholesterol. In ASCOT-LLA (10,305 people with high blood pressure) there were 100 instead of 154 coronary events, the trial ended after 3.3 instead of 5 years. In CARDS (2,838 people with type 2 diabetes) the rate of major events fell from 2.46 to 1.54 per 100 person-years, strokes by 48 percent.¹²

Does the highest study dose bring more?

In TNT researchers compared the highest study dose of 80 mg with the lowest. Major events occurred in 8.7 instead of 10.9 percent, mean LDL was 2.0 instead of 2.6 mmol/l. Persistently raised liver values occurred in 1.2 instead of 0.2 percent, overall mortality was the same.³

What is different after a stroke?

In SPARCL 4,731 people after stroke or TIA received the highest study dose or placebo. Repeat strokes occurred in 11.2 instead of 13.1 percent. On the other hand there were 55 instead of 33 brain bleeds. On balance fewer strokes and cardiovascular events, but the brain bleeds belong in the picture.⁴

What about muscle pain?

In 17 placebo-controlled trials 3.5 percent had muscle pain on atorvastatin and 3.1 percent on placebo. Rarely muscle breakdown with markedly raised CK occurs. According to the label the risk rises with age from 65, with kidney impairment, uncontrolled underactive thyroid, higher dose and interactions.⁵

Why do grapefruit juice and some antibiotics matter?

Atorvastatin is broken down via CYP3A4. Inhibitors of this enzyme such as certain macrolide antibiotics, azole antifungals, ciclosporin and many antiviral drugs raise the level considerably. For grapefruit juice the label names large amounts over 1.2 litres a day. More level means more muscle risk.⁵

Glossary

Terms explained briefly

Dotted words in the text open these explanations directly.

17-alpha-alkylated: Chemical change in oral anabolics that makes them work by mouth and strains liver and blood lipids more.
CK: Creatine kinase, a muscle enzyme in the blood. It rises after hard training and with muscle damage.
Coronary disease: Narrowing of the coronary arteries by deposits, the basis of angina and heart attack.
CYP3A4: Liver enzyme that breaks down many compounds. If something inhibits it, the level of other drugs rises.
Haemorrhagic stroke: Stroke caused by bleeding in the brain, as opposed to an ischaemic stroke from a blocked vessel.
HDL: Cholesterol carrier that brings excess cholesterol back to the liver.
HMG-CoA reductase: Enzyme in the liver that controls the slowest step of the body's own cholesterol production.
LDL: Cholesterol carrier in the blood. High levels are closely linked to deposits in the vessels.
LDL receptor: Docking site on the liver cell through which LDL is taken up from the blood and broken down.
Metabolite: Breakdown product of a compound in the body. Active metabolites keep acting themselves.
Statin: A group of compounds that inhibit the key enzyme of cholesterol production and so lower LDL.
TIA: Transient ischaemic attack: a brief disturbance of blood flow in the brain that resolves on its own.

Evidence

Sources

Show all 7 sourcesHide sources 4 Studies1 Trial registry2 Database checked 26 Oct 2026

Studies

ASCOT-LLA: atorvastatin in high blood pressure with average cholesterol
Sever et al., The Lancet, 2003

DOI 10.1016/S0140-6736(03)12948-0 PMID 12686036

Checked 26 Oct 2026 via doi.org, Crossref, PubMed
CARDS: primary prevention in type 2 diabetes
Colhoun et al., The Lancet, 2004

DOI 10.1016/S0140-6736(04)16895-5 PMID 15325833 NCT00327418

Checked 26 Oct 2026 via doi.org, Crossref, PubMed
TNT: highest versus lowest dose in stable coronary disease
LaRosa et al., New England Journal of Medicine, 2005

DOI 10.1056/NEJMoa050461 PMID 15755765 NCT00327691

Checked 26 Oct 2026 via doi.org, Crossref, PubMed
SPARCL: atorvastatin after stroke or TIA
SPARCL Investigators (Amarenco et al.), New England Journal of Medicine, 2006

DOI 10.1056/NEJMoa061894 PMID 16899775 NCT00147602

Checked 26 Oct 2026 via doi.org, Crossref, PubMed

Trial registry

Trials on atorvastatin on ClinicalTrials.gov
ClinicalTrials.gov, U.S. National Library of Medicine

Checked 26 Oct 2026 via ClinicalTrials.gov API v2

Database

US prescribing information for atorvastatin
DailyMed, U.S. National Library of Medicine (Stand 15.04.2024)

Checked 26 Oct 2026 via DailyMed, openFDA
Mechanism and approval in ChEMBL
ChEMBL, EMBL-EBI (CHEMBL1487, Mechanismus am Calciumsalz CHEMBL393220)

Checked 26 Oct 2026 via ChEMBL