Educational only. Not medical advice. Invite-only research preview.No PHI. Do not share patient names or identifying information (HIPAA).
MytoIntelligence
All targets

Molecular target

α2-Adrenergic Receptor

Also: alpha-2 adrenoceptor · id ALPHA2

Presynaptic autoreceptor regulating norepinephrine release. Agonism reduces sympathetic outflow (clonidine class). Mitragynine has α2-agonist activity contributing to its analgesic and sedative profile.

13 drugs act here2 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 α2-Adrenergic Receptor

These medications have α2-Adrenergic Receptor 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.

AsenapineBrexpiprazoleClonidineEpinephrineGuanfacineLofexidineLurasidoneMirtazapineNorepinephrinePaliperidonePhenoxybenzaminePhentolamineTizanidine

Botanical connections

Plants whose compounds act on α2-Adrenergic Receptor

Each plant below contains a named compound documented to act on α2-Adrenergic Receptor. The compound and the reason for the connection are shown on every edge — a shared mechanism, not a therapeutic equivalence.

Kratom
C
  • MitragynineIndole alkaloid

    Primary alkaloid (~60% of total alkaloid content). Partial μ-opioid agonist + κ-antagonist + α2-adrenergic agonist. Lower-grade serotonergic activity contributes to serotonin-syndrome risk with SSRIs.

  • PaynantheineIndole alkaloid

    Adrenergic-active alkaloid contributing to autonomic effects.

Yohimbe
B
  • YohimbineIndole alkaloid

    Selective α2-adrenergic antagonist — increases sympathetic outflow and norepinephrine release. The pharmacology is the basis for the ED indication and the cardiovascular/anxiety side-effect profile.

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.