1. 8-hydroxy-2,2,14,14-tetramethylpentadecanedioic Acid
2. Esp-55016
3. Esp55016
4. Etc-1002
5. Nexletol
6. Nilemdo
1. Etc-1002
2. 738606-46-7
3. 8-hydroxy-2,2,14,14-tetramethylpentadecanedioic Acid
4. Nexletol
5. Esp-55016
6. Nilemdo
7. Etc1002
8. Etc 1002
9. Esp 55016
10. 1ej6z6q368
11. Mfcd18800820
12. Etc-1002;esp-55016
13. Pentadecanedioic Acid, 8-hydroxy-2,2,14,14-tetramethyl-
14. Bempedoate
15. Unii-1ej6z6q368
16. Bempedoic Acid [usan:inn]
17. Bempedoic-acid
18. Bempedoic Acid
19. Esp-55016
20. Acido Bempedoico
21. Acide Bempedoique
22. Acidum Bempedoicum
23. Nexletol (tn)
24. Bempedoic Acid (usan/inn)
25. Bempedoic Acid [inn]
26. Bempedoic Acid [jan]
27. Bempedoic Acid [usan]
28. Schembl185768
29. Gtpl8321
30. Bempedoic Acid [who-dd]
31. Chembl3545313
32. Chebi:149601
33. Dtxsid401027952
34. Amy31933
35. Bcp16083
36. Esp55016
37. Ex-a1243
38. Zinc3948738
39. Bempedoic Acid [orange Book]
40. S7953
41. Akos027439916
42. Ccg-267969
43. Cs-3952
44. Db11936
45. Nexlizet Component Bempedoic Acid
46. Ac-29040
47. As-49804
48. Hy-12357
49. Sy244715
50. Bempedoic Acid Component Of Nexlizet
51. Bempedoic Acid(etc-1002;esp-55016)
52. Db-108321
53. D10691
54. N10681
55. A905695
56. Q27075007
57. 8-hydroxy-2,2,14,14-tetramethylpentadecanedioic Acid;etc-1002
| Molecular Weight | 344.5 g/mol |
|---|---|
| Molecular Formula | C19H36O5 |
| XLogP3 | 4.8 |
| Hydrogen Bond Donor Count | 3 |
| Hydrogen Bond Acceptor Count | 5 |
| Rotatable Bond Count | 14 |
| Exact Mass | 344.25627424 g/mol |
| Monoisotopic Mass | 344.25627424 g/mol |
| Topological Polar Surface Area | 94.8 Ų |
| Heavy Atom Count | 24 |
| Formal Charge | 0 |
| Complexity | 351 |
| Isotope Atom Count | 0 |
| Defined Atom Stereocenter Count | 0 |
| Undefined Atom Stereocenter Count | 0 |
| Defined Bond Stereocenter Count | 0 |
| Undefined Bond Stereocenter Count | 0 |
| Covalently Bonded Unit Count | 1 |
Bempedoic acid is indicated as an adjunct to diet and maximally tolerated statin therapy for adults with heterozygous familial hypercholesterolemia or existing atherosclerotic cardiovascular disease that warrants additional lowering of LDL-C. The combination of bempedoic and ezetimibe is also indicated with diet management and maximally tolerated statin therapy to treat elevated LDL-C levels in adults with heterozygous familial hypercholesterolemia or existing atherosclerotic cardiovascular disease who require further lowering of LDL-C.
FDA Label
Nilemdo is indicated in adults with primary hypercholesterolaemia (heterozygous familial and non familial) or mixed dyslipidaemia, as an adjunct to diet:
- in combination with a statin or statin with other lipid-lowering therapies in patients unable to reach LDL C goals with the maximum tolerated dose of a statin (see sections 4. 2, 4. 3, and 4. 4) or,
- alone or in combination with other lipid-lowering therapies in patients who are statin intolerant, or for whom a statin is contraindicated.
Bempedoic acid inhibits the synthesis of cholesterol in the liver, reducing LDL-C levels. This reduces the development of atherosclerotic plaques that may increase the risk of cardiovascular events. Earlier clinical trials studying the effects of bempedoic acid showed a dosedependent reduction of LDLC levels in addition to decreased LDL particle number, and reduced levels of apolipoprotein B, nonHDL cholesterol, and highsensitivity Creactive protein. Due to its unique mechanism of action, bempedoic acid is not associated with myositis, an adverse effect that frequently accompanies statin therapy. More recent trials have supported that this drug significantly decreases LDL-C levels after 12 weeks of therapy and provides additional lowering of LDL-C when combined with ezetimibe and statin therapy. The effects of bempedoic acid on mortality are currently unknown.
Enzyme Inhibitors
Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction. (See all compounds classified as Enzyme Inhibitors.)
Hypoglycemic Agents
Substances which lower blood glucose levels. (See all compounds classified as Hypoglycemic Agents.)
Hypolipidemic Agents
Substances that lower the levels of certain LIPIDS in the BLOOD. They are used to treat HYPERLIPIDEMIAS. (See all compounds classified as Hypolipidemic Agents.)
C10AX
C - Cardiovascular system
C10 - Lipid modifying agents
C10A - Lipid modifying agents, plain
C10AX - Other lipid modifying agents
C10AX15 - Bempedoic acid
Absorption
Bempedoic acid is rapidly absorbed in the small intestine. The Tmax of the 180mg tablet is estimated at 3.5 hours.
Route of Elimination
Bempedoic acid's conjugates are primarily eliminated via the urine (70%) and the feces (30%). A total of 5% of the unchanged drug is excreted in the urine and feces, combined.
Volume of Distribution
The apparent volume of distribution of bempedoic acid is about 18L.
Clearance
The clearance (CL/F) of bempedoic acid at steady state was estimated at 11.2 mL/min during clinical trials.
The two main metabolites of bempedoic metabolism are ETC-1002-CoA and ESP15228. Bempedoic acid is primarily eliminated via the metabolism of its acyl glucuronide. This drug is reversibly converted to an active metabolite (ESP15228) based on observations during in vitro studies. Both compounds resulting from the metabolism of bempedoic acid are metabolized to become inactive glucuronide conjugates by the enzyme UGT2B7.
The half-life of bempedoic acid ranges between 15 and 24 hours. Prescribing information indicates a clearance of 21 hours +/- 11 hours.
Normally, LDL cholesterol is produced in the liver and circulates in the blood. When the blood becomes saturated, excess LDL deposits in blood vessels including the coronary arteries, increasing the risk of cardiovascular events. Bempedoic acid is a prodrug that requires activation in the liver. The very-long-chain acyl-CoA synthetase-1 (ACSVL1) enzyme is responsible for its activation to ETC-1002-CoA, the pharmacologically active metabolite. ATP lyase (also known as ATP synthase) plays an important part of cholesterol synthesis. BETC-1002-CoA directly inhibits this enzyme after the parent drug is activated in the liver by coenzyme A (CoA). This inhibition leads to upregulation of the LDL cholesterol receptor, reducing serum LDL-C via increased uptake and LDL clearance in the liver. By the above mechanisms, bempedoic acid causes a total decrease of circulating LDL-C that normally damages blood vessels and leads to atherosclerosis. Lastly, ETC-1002 activates AMP-activated protein kinase (AMPK) in rodents, which inhibits the synthesis of cholesterol via the inhibition of HMG-CoA reductase. The relevance of this to humans is unknown.
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