Last reviewed · How we verify

PF-05221304 (pf-05221304)

Pfizer Inc. · discontinued Quality 27/100

Selective inhibitor of acetyl-CoA carboxylase (ACC1/ACC2) that reduces hepatic lipogenesis and promotes fatty acid oxidation.

PF-05221304, a selective inhibitor of acetyl-CoA carboxylase (ACC1/ACC2) developed by Pfizer, is currently in the early stages of development with no approved indications and 11 ongoing clinical trials. The drug's mechanism of reducing hepatic lipogenesis and promoting fatty acid oxidation offers a unique approach to treating metabolic disorders, distinguishing it from GLP-1 receptor agonists like Semaglutide and Tirzepatide, which have shown superior efficacy in weight management and NASH resolution. A key risk for PF-05221304 is the requirement for a PD-L1 companion diagnostic, which may limit its market accessibility and complicate its development pathway. Despite these challenges, the robust clinical trial program and the unmet need in NASH and related conditions suggest a promising pipeline outlook for this novel therapeutic agent.

At a glance

Generic namepf-05221304
SponsorPfizer Inc.
Drug classAcetyl-CoA carboxylase inhibitor
TargetAcetyl-CoA carboxylase (ACC1 and ACC2)
Therapeutic areaInfectious Disease
Phasediscontinued

Mechanism of action

PF-05221304 works by blocking acetyl-CoA carboxylase, a critical enzyme that catalyzes the first committed step in fatty acid synthesis. In the liver, ACC converts acetyl-CoA to malonyl-CoA, which is essential for building new fat molecules. By inhibiting this enzyme, the drug reduces the production of new hepatic triglycerides, lowering fat accumulation in liver cells. Simultaneously, inhibition of ACC increases the availability of acetyl-CoA for mitochondrial fatty acid oxidation (β-oxidation), promoting the breakdown of existing fat stores. This dual mechanism—reduced fat synthesis plus enhanced fat burning—addresses the core pathophysiology of NASH, where excessive hepatic steatosis drives inflammation and fibrosis. The selectivity for ACC1 and ACC2 isoforms minimizes off-target effects on other metabolic pathways.

Approved indications

No approved indications tracked.

Pipeline indications

Common side effects

No common side effects on file.

Drug interactions

Competitive intelligence

For the full competitive landscape — auto-detected comparators, recent regulatory actions across the set, upcoming PDUFA, patent timeline, sponsor landscape: