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MytoIntelligence
All targets

Molecular target

L-Type Voltage-Gated Calcium Channel

Calcium channel critical for vascular smooth muscle contraction and cardiac conduction. Antagonism by dihydropyridine CCBs (amlodipine, nifedipine) preferentially relaxes vasculature; non-DHP CCBs (verapamil, diltiazem) also slow cardiac conduction.

14 drugs act here5 plants reach it via their compounds

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 L-Type Voltage-Gated Calcium Channel

These medications have L-Type Voltage-Gated Calcium Channel 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 L-Type Voltage-Gated Calcium Channel

Each plant below contains a named compound documented to act on L-Type Voltage-Gated Calcium Channel. The compound and the reason for the connection are shown on every edge — a shared mechanism, not a therapeutic equivalence.

  • KhellinFurochromone

    Khellin has been reported to inhibit L-type voltage-gated calcium channels, producing smooth-muscle relaxation in bronchial and vascular tissues; it is also reported to stabilise mast cells, reducing mediator release. These mechanisms are considered the pharmacological basis for khellin's structural inspiration for the development of cromolyn sodium and nifedipine, per review literature.

  • VisnaginFurochromone

    Visnagin shares calcium-channel-modulating properties with khellin; in vitro studies report that visnagin, alongside khellin, may reduce oxalate-induced renal epithelial cell damage, with a proposed mechanism involving modulation of calcium-dependent cellular injury pathways.

  • Berbaminebisbenzylisoquinoline alkaloid

    Calcium-channel modulating activity contributes to mild antiarrhythmic and vasodilatory effects observed in preclinical models.

  • Panax notoginseng saponins (PNS) — notoginsenoside R1, ginsenoside Rb1, ginsenoside Rg1Triterpenoid saponins

    Studies report multi-target activity: inhibition of NF-κB–mediated neuroinflammation, modulation of thromboxane A2 and arachidonic acid pathways to attenuate platelet aggregation, nitric oxide/cGMP pathway modulation, NMDA receptor involvement in neuroprotection, and L-type calcium channel effects relevant to cardiovascular research contexts.

  • 3-n-Butylphthalide (NBP)Phthalide

    Proposed mechanisms include vasodilatory activity via calcium channel modulation, nitric oxide/cGMP pathway enhancement, and ACE inhibition; anxiolytic and antidepressant-related activity investigated in preclinical models via GABAergic and serotonergic pathways. Clinical data from Shayani Rad et al. (2022, 2023) investigated these effects in hypertensive patients.

  • Tanshinone IIAditerpenoid quinone

    Calcium-channel modulating activity contributes to vasodilation, anti-arrhythmic, and the anti-fibrotic effects observed in cardiac trials.

A shared molecular target shows how a botanical and a drug relate mechanistically. It is not evidence that one can replace the other. Educational summary only — discuss any medication decision with your clinician.