Bempedoic acid inhibits ATP citrate lyase (ACL), an enzyme which converts Citrate to Acetyl CoA . After this step, the pathway is same i.e. Acetyl CoA to HMG CoA and mevalonate (targeted by statins) and cholesterol. My questions are:-
1) If the downstream pathway is same, why this compound is considered as an effective option?
2) We do have additional LDL lowering option (if statins are not effective) e.g. ranging from Ezetimibe to PCSK9 inhibitors. Then what is the added advantage of Bempedoic acid over these options?
3) Are there any special patient groups which respond more to this compound?
Thank you for this question.
If oxidized small dense LDL (oxsdLDL) is bad, with sdLDL unable to bind with CD36, and therefore in the serum much longer to oxidize, and oxidized sdLDL is at even higher risk for becoming glycosylated, so that oxidized, glycolylated sd LDL s the primary form of LDL that penetrates the endolumin in order for foam cells to form...
.... can you help me understand why just LDL is worth attention?
$8 Billion in pharmaceutical revenue depends on LDL remaining some object of evil.
Besides, that, however, can you educate me on how LDL outside of sdLDL or oxLDL or glycosylatedLDL is any kind of problem?
Thanks!
Eric Klein Thank you for your thought provoking reply. However, my query is entirely different. I understand your concern but I am looking for a different answer. So far according to ACC/AHA, LDL reduction by statins is considered as a major positive impact on CAD. I simply want to ask if the downstream pathway is same for bempedoic acid and statins, what is the relevance of developing bempedoic acid. Thank you.
Thanks for the interesting question.
I think based on the latest available evidence I came across, bempedoic acid has shown a further reduction in LDL-C in patients who already on ezetimibe and on lowest statin dose or intolerant to statins. So it just an appealing option in case of needed further LDL-C reduction on top of statin and ezetimibe.
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