Bempedoic Acid Research Grade Compound (ACL Inhibitor) Supplier — UPOR Biotech
Bempedoic Acid (ETC-1002, CAS 738606-46-7) — a first-in-class ATP citrate lyase (ACL) inhibitor that blocks hepatic cholesterol synthesis upstream of HMG-CoA reductase to drive clinically significant LDL-C reduction. A liver-targeted prodrug with a muscle-sparing profile and AMPK activation — delivered as a Research Grade (RUO) reference compound. C₁₉H₃₆O₅, MW 344.49 g/mol — bulk supplier and reference standard from UPOR Biotech.
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Bempedoic acid (CAS 738606-46-7, C₁₉H₃₆O₅, MW 344.49 g/mol) is a first-in-class ATP citrate lyase (ACL/ACLY) inhibitor and a substituted dicarboxylic-acid small molecule (referenced commercially as Nexletol — positioned here strictly as a research reference standard). In the liver, bempedoic acid is converted to its active thioester metabolite bempedoyl-CoA, which inhibits ATP-citrate lyase with an IC₅₀ of ~29 µM. Because ACL converts citrate to acetyl-CoA and oxaloacetate — the rate-limiting supply step for hepatic cholesterol and fatty-acid synthesis — ACL inhibition depletes the acetyl-CoA pool feeding downstream HMG-CoA reductase and de-novo lipogenesis, thereby lowering LDL cholesterol. Bempedoic acid also activates AMP-activated protein kinase (AMPK), an energy sensor that further suppresses lipid synthesis and promotes fatty-acid oxidation. Its liver-targeted prodrug mechanism — the active CoA metabolite is generated almost exclusively in hepatocytes — spares skeletal muscle, underpinning the muscle-sparing profile (no myopathy) reported in reference clinical studies.
As a Research Grade (RUO) compound for the study of LDL-C lowering and cholesterol-synthesis pharmacology, bempedoic acid is an essential tool for hypercholesterolemia research, statin-refractory lipid-lowering studies, and ACL-mediated lipogenesis investigations. It is commonly co-studied with statins (HMG-CoA reductase inhibitors) and ezetimibe in combination lipid-pharmacology work. Research Use Only (RUO) — not for human diagnostic or therapeutic use. UPOR Biotech provides full documentation — COA (HPLC ≥98.0%), MSDS, HPLC chromatogram, and heavy-metals data — backed by ISO 9001, cGMP, and FDA facility registration. Available in research packaging: 1 g / 5 g / 10 g / 50 g.
Bempedoic Acid vs Statins — ACL Inhibition vs HMG-CoA Reductase Inhibition
The central comparison in cholesterol-lowering pharmacology: bempedoic acid targets ATP-citrate lyase upstream of HMG-CoA reductase, reducing the acetyl-CoA supply to hepatic cholesterol synthesis, whereas statins directly block HMG-CoA reductase, the downstream rate-limiting enzyme. Because bempedoic acid acts predominantly in the liver through its prodrug (bempedoyl-CoA) and spares muscle, it offers a muscle-sparing profile versus the myalgia associated with statin therapy. The two mechanisms are commonly co-studied in LDL-C lowering research — bempedoic acid is frequently combined with statins or ezetimibe in reference trials to achieve additive LDL-C reduction. For researchers, the distinction between upstream (ACL) and downstream (HMG-CoA reductase) inhibition defines the complementary arms of lipid-metabolism pharmacology.
Technical Specifications
| Property | Specification |
|---|---|
| Product Name | Bempedoic Acid — Research Grade (RUO) — ATP Citrate Lyase (ACL) Inhibitor Reference Compound |
| Synonyms | Bempedoic Acid; ETC-1002; ESP-55016 |
| CAS Number | 738606-46-7 |
| Molecular Formula | C₁₉H₃₆O₅ |
| Molecular Weight | 344.49 g/mol |
| IUPAC Name | 8-Hydroxy-2,2,14,14-tetramethylpentadecanedioic acid |
| Compound Class | Small-molecule dicarboxylic acid; first-in-class ATP citrate lyase (ACL/ACLY) inhibitor |
| Mechanism of Action | Inhibition of hepatic ATP-citrate lyase (IC₅₀ ~29 µM) reduces acetyl-CoA supply for cholesterol and fatty-acid synthesis, lowering LDL-C; activates AMP-activated protein kinase (AMPK) |
| Active Metabolite | Bempedoyl-CoA — liver-targeted prodrug activation spares skeletal muscle (no myopathy in reference studies) |
| Target Enzyme | ATP citrate lyase (ACLY) |
| Purity (HPLC) | ≥98.0% |
| Appearance | White to off-white crystalline solid |
| Melting Point | ~68–70°C |
| Solubility | DMSO ≥50 mg/mL; soluble in methanol, ethanol, and DMF |
| Heavy Metals (Total) | ≤10 ppm |
| Residual Solvents | Meets ICH Q3C requirements |
| Water Content (KF) | ≤1.0% |
| Related Substances | Each individual impurity ≤0.5% by HPLC |
| Storage | 2–8°C, tightly sealed, protected from light and moisture |
| Grade | Research Grade (RUO) — reference standard |
| Regulatory Status | For research use only; not for human diagnostic or therapeutic use |
| Applications | LDL-C reduction research, statin-refractory lipid-lowering studies, ACL-mediated lipogenesis, AMPK signaling, combination lipid pharmacology |
| Origin / Manufacture | Synthesized under cGMP-compliant conditions; analytical reference-standard grade |
| Certifications | ISO 9001:2015, cGMP, FDA facility registration |
| Packaging | 1 g / 5 g / 10 g / 50 g |
| Shelf Life | 3 years |
| Disclaimer | Research Use Only (RUO) — not for human diagnostic or therapeutic use |
Key Benefits — Bempedoic Acid Research Grade
First-in-Class ATP Citrate Lyase Inhibition
Bempedoic acid is the first-in-class ATP citrate lyase (ACL/ACLY) inhibitor — blocking the committed supply step for hepatic cholesterol and fatty-acid synthesis. Its prodrug mechanism concentrates the active bempedoyl-CoA metabolite in hepatocytes, enabling liver-selective lipid-synthesis inhibition.
First-in-Class ACLReduces Hepatic Cholesterol Synthesis (IC₅₀ ~29 µM)
ACL inhibition with IC₅₀ ~29 µM depletes the acetyl-CoA pool feeding downstream cholesterol biosynthesis, producing clinically significant LDL-C reduction in reference studies. Effective in statin-refractory and statin-intolerant research models.
LDL-C LoweringAMPK Activation & Muscle-Sparing Profile
Bempedoic acid activates AMP-activated protein kinase (AMPK), suppressing lipogenesis and promoting fatty-acid oxidation. The liver-targeted prodrug mechanism spares skeletal muscle — no myopathy in reference clinical studies.
Muscle-Sparing≥98% HPLC Purity Reference Standard
Supplied as a Research Grade (RUO) reference standard with ≥98.0% HPLC purity, ≤10 ppm heavy metals, and full COA documentation — suitable for analytical method development, bioassay, and combination lipid-pharmacology research.
Reference StandardApplications
Hypercholesterolemia & LDL-C Reduction Research
Primary application — ACL inhibition studies targeting LDL-C lowering and hepatic cholesterol-synthesis blockade in hypercholesterolemia and dyslipidemia models. Reference-standard compound for lipid-metabolism screening.
Statin-Refractory Lipid-Lowering Studies
Second-line lipid-lowering research — bempedoic acid for statin-intolerant and statin-refractory models, complementing HMG-CoA reductase blockade with upstream ACL inhibition for additive LDL-C reduction.
ACL-Mediated Lipogenesis & De-Novo Synthesis Research
Investigate ACL-mediated de-novo lipogenesis and the acetyl-CoA/malonyl-CoA axis in hepatocytes — key to hepatic steatosis, lipid homeostasis, and metabolic-disease research.
AMPK Signaling Pathway Studies
Tool compound for AMPK activation research — studying energy-sensing pathways, fatty-acid oxidation, and crosstalk between ACL inhibition and AMPK-mediated metabolic signaling.
Combination Lipid Pharmacology (with Statins/Ezetimibe)
Combination lipid pharmacology — co-studied with statins (HMG-CoA reductase inhibitors) and ezetimibe (NPC1L1 blocker) in reference trials for additive and complementary LDL-C lowering.
Analytical Reference Standard & Method Development
Reference standard for HPLC method development, calibration curves, and impurity profiling of bempedoic acid in drug-substance and formulation research — with COA and HPLC chromatogram supplied.
Frequently Asked Questions
Bempedoic acid (ETC-1002, ESP-55016, CAS 738606-46-7) is a first-in-class ATP citrate lyase (ACL/ACLY) inhibitor and a dicarboxylic-acid small molecule. In the liver it is converted to bempedoyl-CoA, which inhibits ACL with IC₅₀ ~29 µM, blocking hepatic cholesterol synthesis by reducing the acetyl-CoA supply for downstream cholesterol and fatty-acid biosynthesis. It also activates AMPK, and the liver-targeted prodrug mechanism spares skeletal muscle. Together these actions drive clinically significant LDL-C reduction in reference studies.
Statins block HMG-CoA reductase — the downstream rate-limiting enzyme of cholesterol synthesis — whereas bempedoic acid inhibits ATP-citrate lyase upstream, reducing the acetyl-CoA supply that feeds cholesterol synthesis. Bempedoic acid’s liver-targeted prodrug mechanism spares muscle (no myopathy in reference studies), distinguishing it from the myalgia profile of statins. The mechanisms are complementary and commonly co-studied for additive LDL-C lowering in combination lipid pharmacology.
Core applications include LDL-C lowering and hypercholesterolemia research, statin-refractory lipid-lowering studies, ACL-mediated lipogenesis and de-novo synthesis research, AMPK signaling studies, combination lipid pharmacology (with statins/ezetimibe), and use as an analytical reference standard for HPLC method development.
Store at 2–8°C, tightly sealed and protected from light and moisture. Prepare stock solutions in DMSO (≥50 mg/mL) and dilute to working concentrations in aqueous buffer for assays. Use appropriate personal protective equipment and handle in a fume hood. Stored correctly, the compound maintains ≥98% purity for its 3-year shelf life.
Every shipment includes COA (HPLC ≥98.0%, related substances, heavy metals ≤10 ppm), MSDS, HPLC chromatogram, and lot-specific documentation — backed by ISO 9001, cGMP, and FDA facility registration. Material is supplied as Research Grade (RUO) — not for human diagnostic or therapeutic use.