Akuammidine (Akuamma Indole Alkaloid · Mu-Opioid Agonist · Informational)
Compiled from published pharmacological and botanical literature. Not independently verified by Herbuno. Spotted an error or have a correction? Flag it below →
| Compound | Akuammidine (Rhazine) |
| Chemical class | Alkaloid — Indole (sarpagine-type monoterpenoid indole alkaloid) |
| CAS | 639-38-3 |
| Primary source | Picralima nitida (akuamma) seeds — minor alkaloid |
| Key applications | Mu-opioid receptor agonist; research context; informational-only |
| Claim strength | Emerging |
| Typical form | Research reference; not offered as a supplement ingredient |
| Buy from Herbuno | Informational reference — see HerbIQ Compound Index → |
Name origin: Akuammidine, also known as rhazine, derives its name from akuamma, the West African name for Picralima nitida, in common with the whole akuamma alkaloid family. Structurally it belongs to the sarpagine class of monoterpenoid indole alkaloids — the same skeleton documented elsewhere in HerbIQ under sarpagine itself — which distinguishes it from the akuammiline-type alkaloids that dominate the seed. Traditional use: Akuamma seeds have long been used in West African, particularly Ghanaian, traditional medicine for pain, fever, and malaria, and a crude seed extract was reported to have antinociceptive activity described as comparable to morphine, an effect partially reversed by naloxone. That naloxone reversal was the first clear signal that the seed's analgesic reputation had a genuine opioid basis, and it prompted the search for which alkaloids were responsible. Research trajectory: Akuammidine emerged from that search as the akuamma alkaloid with the clearest mu-opioid agonist profile. Radioligand binding and isolated-tissue work established its preference for mu-opioid sites and confirmed, through blockade by naloxone and by a selective mu antagonist, that its agonist actions are genuinely mu-mediated Menzies 1998. Later work isolating six akuamma alkaloids in high purity and screening them across a receptor panel confirmed that the opioid receptors are the primary target of this alkaloid family Creed 2021. Safety context: As a mu-opioid agonist, akuammidine carries the dependence and safety considerations of opioid-active compounds; it is documented here as a factual research reference and is not offered as an ingredient.
Evidence for Akuammidine Applications
Mu-opioid agonism: Akuammidine showed a preference for mu-opioid binding sites with a Ki of approximately 0.6 micromolar, compared with 2.4 micromolar at delta and 8.6 micromolar at kappa sites, and its agonist actions in the mouse-isolated vas deferens were antagonised both by naloxone and by the selective mu-opioid antagonist CTOP, confirming a genuine mu-receptor action Menzies 1998. This makes it the most clearly agonist member of the akuamma group at the mu receptor. Claim strength: Emerging.
Low affinity in absolute terms: Although akuammidine prefers the mu site, its affinity there corresponds to a value roughly 400-fold lower than that of a highly selective mu-opioid ligand, so its potency is modest and it should not be equated with a conventional opioid analgesic Menzies 1998. Claim strength: Emerging.
Part of an opioid-targeting alkaloid family: Receptor-panel screening of the purified akuamma alkaloids against more than 40 CNS targets confirmed that the opioid receptors are the primary targets of this family as a whole, situating akuammidine's mu activity within a coherent group pharmacology rather than as an isolated finding Creed 2021. Claim strength: Emerging.
Divergent activities within the family: The akuamma alkaloids are pharmacologically heterogeneous despite their shared origin — akuammidine acts as a mu-preferring agonist while akuammine has been reported as a mu antagonist and akuammicine as a kappa agonist — which means the effects of whole-seed material reflect a mixture of opposing and complementary opioid actions Menzies 1998. Claim strength: Emerging.
Minor abundance: Akuammidine is present in akuamma seed at levels far below akuammine; a commercial 250 mg seed capsule has been estimated to contain on the order of 1.4 mg akuammine but only about 0.085 mg akuammidine, so its contribution to whole-seed pharmacology is limited by abundance as well as by potency Menzies 1998. Claim strength: Emerging.
This compound is documented for research and formulator education purposes. For commercially available botanical ingredients, explore the HerbIQ Compound Index →
Dosage & Formulator Specification
Akuammidine is documented here for research and formulator education only; Herbuno does not offer it as an ingredient, and no established human dose exists. As a mu-opioid receptor agonist it falls outside the botanical ingredient range, and no supplement-grade akuammidine material exists.
The abundance data matter for anyone interpreting akuamma seed products. Akuammidine is a minor constituent, present at roughly a twentieth of the akuammine content in commercial seed preparations, so the alkaloid with the clearest mu-agonist activity is also one of the least abundant. This mismatch between potency profile and abundance is a central difficulty in attributing the traditional analgesic effect of the seed to any single constituent, and it argues strongly for full alkaloid profiling rather than single-marker characterisation of any akuamma material.
The pharmacological heterogeneity of the family compounds this. Because akuammidine is a mu-preferring agonist, akuammine has been reported as a mu antagonist, and akuammicine is a kappa agonist, whole-seed material delivers a mixture of opposing opioid actions whose net effect cannot be predicted from any one alkaloid. Responsible discussion of akuamma seed must engage with that complexity rather than reducing the material to a single active.
This monograph provides chemical, pharmacological, and safety context within the HerbIQ index, situating akuammidine alongside the other akuamma alkaloids and the sarpagine-type alkaloids covered elsewhere, and does not constitute sourcing guidance.
Frequently Asked Questions — Akuammidine
What is akuammidine?
Akuammidine is a sarpagine-type monoterpenoid indole alkaloid of Picralima nitida (akuamma) seeds. Among the akuamma alkaloids it is notable as the one showing the clearest mu-opioid agonist behaviour, though its affinity remains in the micromolar range.
How does akuammidine act at opioid receptors?
In radioligand binding and isolated-tissue assays, akuammidine showed a preference for mu-opioid binding sites with a Ki of about 0.6 micromolar, versus 2.4 and 8.6 micromolar at delta and kappa sites. Its agonist actions in the mouse vas deferens were blocked by naloxone and by a selective mu antagonist, confirming a genuine action at mu-opioid receptors.
Why is akuammidine informational-only?
It is a mu-opioid agonist, and compounds with opioid activity carry dependence and safety considerations that place them outside Herbuno's botanical ingredient range. This page documents akuammidine factually as a research and chemical-family reference.
Is akuammidine abundant in akuamma seed?
No. Akuammidine is a minor constituent relative to akuammine, which dominates the seed alkaloid profile. Commercial akuamma seed preparations deliver akuammidine at levels far below akuammine, which is one reason the pharmacology of the whole seed is difficult to attribute to any single alkaloid.
Related compounds: Akuammine, Akuammicine, Sarpagine, Mitragynine
Claim-strength scale – High = multiple human RCTs; Moderate = limited trials or strong preclinical convergence; Emerging = early-stage lab or animal data.
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