Molecular target
HMG-CoA Reductase
Rate-limiting enzyme in cholesterol biosynthesis. Inhibition lowers LDL cholesterol and is the mechanism of statins. Red yeast rice contains naturally occurring monacolin K — chemically identical to lovastatin — making it the single most direct plant-to-drug mechanism overlap on this site.
Educational use only. This page summarizes published research and traditional-use records for educational purposes. It does not diagnose, treat, cure, or prevent any disease. Do not start, stop, or change medications based on this information. Discuss any decisions about therapies — pharmaceutical or botanical — with a qualified clinician who knows your medical history.
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Pharmaceutical agents
Drugs that act on HMG-CoA Reductase
These medications have HMG-CoA Reductase among their molecular targets. Sharing a target is a mechanistic relationship — it does not make any plant below an alternative to, or substitute for, these drugs.
Botanical connections
Plants whose compounds act on HMG-CoA Reductase
Each plant below contains a named compound documented to act on HMG-CoA Reductase. The compound and the reason for the connection are shown on every edge — a shared mechanism, not a therapeutic equivalence.
- Monacolin KStatin (polyketide)
Chemically identical to lovastatin. This is not 'statin-like' — it IS a statin in plant form. Carries the same mechanism, same myopathy/rhabdomyolysis risk, and same contraindications as the prescription drug.
- Other monacolinsStatin (polyketide)
Secondary monacolins (J, L, M, X) contributing to total HMG-CoA inhibition.
- β-SitosterolPhytosterol
Reviewed studies report β-sitosterol may competitively inhibit cholesterol absorption and interact with HMG-CoA reductase pathway; predominantly in vitro and animal data (Olas et al. 2024; Bhuyan et al. 2019)
- Bergamot Polyphenolic Fraction (BPF)Mixed flavonoid extract
Standardized polyphenolic fraction containing brutieridin and melitidin — naturally occurring statin-like flavonoid glycosides with milder HMG-CoA inhibition than monacolin K.
- Luteolin (and artichoke leaf extract phenolics)
Artichoke leaf extract phenolics, with luteolin identified as an active constituent, have been shown to inhibit hepatic cholesterol biosynthesis by indirect modulation/inhibition of HMG-CoA reductase activity in hepatocyte studies. This is the documented mechanism behind the modest LDL reduction (~7%, Bundy 2008 RCT). Claim-safe: in vitro/mechanistic support; clinical effect is modest.
- Guggulsterones (Z- and E-isomers)Steroidal ketones
Studies report guggulsterones modulate bile acid receptor (FXR) antagonism, suppress NF-κB signalling, inhibit 5-lipoxygenase, and have been reported to influence thyroid hormone receptor activity and HMG-CoA reductase pathway — proposed contributors to observed lipid-modulating effects in clinical studies.