Molecular target
β2-Adrenergic Receptor
Smooth-muscle adrenergic receptor; agonism causes bronchodilation and vasodilation. Non-selective beta-blockers (propranolol) antagonize both β1 and β2, contributing to their bronchospasm risk in asthma but also to the off-label anxiolytic / migraine prophylactic effects.
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 β2-Adrenergic Receptor
These medications have β2-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.
Botanical connections
Plants whose compounds act on β2-Adrenergic Receptor
Each plant below contains a named compound documented to act on β2-Adrenergic Receptor. The compound and the reason for the connection are shown on every edge — a shared mechanism, not a therapeutic equivalence.
- Ephedrinephenethylamine alkaloid
Indirect-acting sympathomimetic (releases norepinephrine from sympathetic nerve terminals) plus direct α1, β1, β2 adrenergic agonism. The combination produces vasoconstriction, increased cardiac output, and bronchodilation — therapeutic for bronchospasm and decongestion but at significant cardiovascular cost.
- Pseudoephedrinephenethylamine stereoisomer
Stereoisomer of ephedrine with greater nasal-decongestant selectivity — the basis for FDA-permitted single-ingredient pseudoephedrine OTC products (Sudafed). Lower cardiovascular impact than ephedrine but still meaningful at high dose.
- Alpha-hederinTriterpenoid saponin
In vitro research (HEK293 and A549 cell lines) reported that alpha-hederin inhibited agonist-induced internalisation of β2-adrenergic receptors, which may increase receptor surface availability; hederacoside C and hederagenin did not reproduce this effect at the same concentrations (Sieben et al., 2009).