Apomorphine
Apomorphine HCl
Apomorphine (Apomorphine HCl) is a hormonal & sexual research compound. Non-selective dopamine agonist acting centrally at the paraventricular nucleus — it drives erection through the brain rather than through vascular smooth muscle, which is a completely different route from a PDE5 inhibitor.
Apomorphine quick facts
| Reported research dose | 2–3mg sublingual |
| Route | Sublingual |
| Frequency | 1x · As needed |
| Half-life | ~40 minutes |
| Forms | Oral |
| Evidence level | Was approved in Europe as Uprima; withdrawn commercially rather than for safety |
Despite the name it is not an opioid and has no morphine activity. The central mechanism means it can work where PDE5 inhibitors don't — but nausea is the dose-limiting effect and it's why the drug failed commercially. Safe alongside nitrates, unlike PDE5 inhibitors, which is its one clear niche.
How Apomorphine works
Non-selective dopamine agonist acting centrally at the paraventricular nucleus — it drives erection through the brain rather than through vascular smooth muscle, which is a completely different route from a PDE5 inhibitor.
Proposed benefits
Researched for libido, hormonal signaling and reproductive / sexual function.
Where to get Apomorphine
Buy Apomorphine at AlgoRx →The evidence for Apomorphine
Graded by what exists behind each claim.
✅ Clinically validated
- Approved — as a subcutaneous rescue therapy for Parkinson's 'off' episodes, with solid trial data. It was also approved as sublingual Uprima for erectile dysfunction in Europe and later withdrawn commercially, having shown efficacy below the PDE5 inhibitors with substantially more nausea.
📊 Correlative data
- Limited community use, and the reported barrier is exactly what the trials found: nausea is common and frequently dose-limiting, arriving before any useful effect at the doses people try. Where it is used it tends to be by people for whom PDE5 inhibitors did nothing — which is a coherent reason, since the mechanism is unrelated.
🧪 Theoretical / extrapolated
- A non-selective dopamine agonist acting centrally — despite the name it contains no morphine and has no opioid activity.
- Central dopaminergic action on erectile function is a genuinely different mechanism from PDE5 inhibition, which is peripheral and vascular. The same central dopaminergic activity drives the nausea through the chemoreceptor trigger zone, which is why it never displaced the PDE5 drugs.
How to read these tiers: they say how much human evidence exists, not how well something works — and ✗ flags harm, never a disappointing trial. How the evidence tiers work →
What Apomorphine actually does
Start with the name, because it is the most misleading name in the catalog. Apomorphine is made from morphine by an acid-driven rearrangement, and that shared ancestry is the entire connection. It has no opioid activity, does not bind opioid receptors, is not reversed by naloxone and is not a controlled opioid. What the rearrangement produces is an aporphine: a rigid tetracyclic scaffold that presents a catechol — two adjacent hydroxyl groups on an aromatic ring — in almost exactly the geometry dopamine presents its own. The molecule is a locked-conformation dopamine mimic, and every property on this page follows from that one structural fact.
It is not selective, and the lack of selectivity is the point. Jenner 2016 describes apomorphine as a potent, direct and broad-spectrum dopamine agonist activating all dopamine receptor subtypes, with additional affinity for serotonin and α-adrenergic receptors. That separates it cleanly from pramipexole and ropinirole, which are D2/D3-preferring. Dopamine released from a levodopa dose hits the D1 family and the D2 family together; so does apomorphine, which is why it is the one agonist titratable to a levodopa-equivalent antiparkinsonian response Jenner 2016 rather than a partial one.
The vomiting is not a side effect in the ordinary sense. It is the same receptor, in the one place the drug cannot avoid. The area postrema — the chemoreceptor trigger zone in the floor of the fourth ventricle — sits outside the blood-brain barrier and is dense in D2 receptors. Any dopamine agonist that reaches the circulation reaches that structure first, without having to cross anything. So a broad-spectrum agonist given systemically produces emesis before, and at lower exposure than, the central motor or sexual effects people are actually after. Apomorphine was used as a standard emetic in humans and animals for a century before it was a Parkinson’s drug. That is the honest framing: the anti-nausea drug is not managing an inconvenience, it is the only thing that makes the rest of the pharmacology usable.
And that is why the antiemetic used is a strange old one. The obvious antiemetic for a dopamine agonist would be a D2 antagonist — which would block the therapy. The next obvious class is the 5-HT3 antagonists, and those are contraindicated: the label records profound hypotension and loss of consciousness when apomorphine was given with ondansetron, and extends the contraindication to granisetron, dolasetron, palonosetron and alosetron U.S. Food and Drug Administration 2025. What is left is trimethobenzamide, an agent from the 1950s, started three days ahead.
The erectile mechanism is central, and this is the one place the molecule has no competitor. Dopaminergic transmission in the hypothalamic paraventricular nucleus initiates the erectile reflex through a descending oxytocinergic pathway. A PDE5 inhibitor works at the other end of that chain entirely — it stops cyclic GMP being broken down in penile smooth muscle, which requires nitric oxide to have been released in the first place. Apomorphine works upstream, in the brain. That is why it has no nitrate interaction and why it can in principle work where a PDE5 inhibitor does nothing — and also why the dose that reaches the hypothalamus has already saturated the area postrema.
Cell, rodent, human — and where it stops
Step one, the receptor pharmacology. Broad-spectrum activation of every dopamine receptor subtype, with serotonergic and α-adrenergic affinity alongside Jenner 2016.
Step two, humans, subcutaneous, acute — and the effect size is enormous. Dewey 2001 randomized 29 patients with advanced Parkinson’s disease (20 apomorphine, 9 placebo) to subcutaneous injections of 2 to 10 mg during a practically defined off state. The Unified Parkinson’s Disease Rating Scale motor score at 20 minutes fell by 23.9 points (62%) on apomorphine and 0.1 points (1%) on placebo, P < 0.001; 95% of off states were successfully reversed against 23% on placebo. Very few drugs in neurology produce a separation like that.
Step three, humans, continuous subcutaneous infusion, 12 weeks. Katzenschlager 2018 — TOLEDO — randomized 107 patients (106 analyzed, 53 per arm) to apomorphine 3–8 mg/h infused during 16 waking hours a day, or to a saline infusion, for 12 weeks. Daily OFF time fell by 2.47 hours on apomorphine and 0.58 hours on placebo, a treatment difference of 1.89 hours per day, p = 0.0025. Nausea was the most common adverse event.
Step four, humans, sublingual film — it works, and the mouth is the price. Olanow 2020 randomized 109 patients to apomorphine sublingual film 10–35 mg or placebo. The MDS-UPDRS part 3 motor score 30 minutes after dosing at week 12 fell 11.1 points against 3.5 on placebo, p = 0.0002. But only 34 of 54 (63%) on apomorphine completed the study against 46 of 55 (84%) on placebo, and mild-to-moderate oropharyngeal events occurred in 17 of 54 (31%), with nausea in 28%, somnolence 13% and dizziness 9%.
Step five, the other indication, and the reason the drug is on a research site at all. Dula 2001 studied 296 heterosexual men with erectile dysfunction in a double-blind crossover of 3 mg sublingual apomorphine against placebo and against 4 mg. 3 mg was significantly more effective than placebo (p < 0.001). The dose-response for the limiting effect is the number to keep: nausea in 3.3% at 3 mg against 14.1% at 4 mg, and 7.0% at 3 mg against 1.1% on placebo. One extra milligram roughly quadrupled the nausea.
The obstacle, stated exactly, and it is a therapeutic-window obstacle rather than a species one. Nothing here failed to translate — every step above is human. What failed is the ratio between the dose that works and the dose that makes you sick, and it failed in the indication where an easier competitor existed. Sublingual apomorphine for erectile dysfunction was approved in Europe as Uprima and withdrawn commercially, with efficacy below the PDE5 inhibitors and substantially more nausea; the same molecule at three to ten times the dose remains approved for Parkinson’s, where the alternative is an hour of immobility and the trade is worth making. The compound did not change. The comparator did.
Apomorphine pharmacokinetics — how much of it actually gets in
Route: injected, or absorbed through a mucosa. There is no oral apomorphine and there cannot easily be one. The molecule is a catechol, and catechols are conjugated in the gut wall and the liver before they reach the circulation. Given subcutaneously the label reports bioavailability equal to that of intravenous administration, with time to peak of 10 to 60 minutes U.S. Food and Drug Administration 2025.
The half-life is the whole clinical personality of this drug. Mean terminal elimination half-life is about 40 minutes (range 30 to 60) U.S. Food and Drug Administration 2025. Do the arithmetic out loud: three half-lives is two hours and leaves about 12% of peak; four is under three hours and leaves about 6%. A rescue drug is what a 40-minute half-life makes possible and a maintenance drug is what it makes impossible, which is why the chronic version of this therapy is a 16-hour-a-day pump Katzenschlager 2018 rather than a tablet.
What degrades it: officially, nobody knows. The label says flatly that the route of metabolism in humans is not known, and lists sulfation, N-demethylation, glucuronidation and oxidation as the possibilities U.S. Food and Drug Administration 2025. Cytochrome P450 plays only a minor role, so apomorphine is neither a meaningful CYP substrate, inhibitor nor inducer, and a pharmacokinetic interaction with COMT inhibitors is described as unlikely. For a drug approved in 2004 that is a genuine hole rather than a technicality: interactions here cannot be reasoned about from first principles because the clearing enzyme has never been named.
One number in the label implies something the label does not say. Mean apparent clearance is 223 L/h (range 125 to 401) with an apparent volume of distribution of 218 L (123 to 404) U.S. Food and Drug Administration 2025. 223 L/h is about 3.7 L/min. Liver blood flow in an adult is roughly 1.5 L/min, so a clearance of 3.7 L/min cannot all be hepatic — the liver cannot remove a drug faster than blood delivers it. Read alongside subcutaneous bioavailability equal to intravenous, the arithmetic points at substantial extrahepatic elimination, probably conjugation in blood and peripheral tissue. That is an inference from two label numbers, clearly offered as one, and it is the most interesting unresolved thing about this molecule’s disposition.
The mucosal route, and how much of it is wasted. Agbo 2021 compared the sublingual film with subcutaneous apomorphine in a randomized three-way crossover: film at 15/20/25/30 mg against subcutaneous at 2/3/4/5 mg, and the film delivered only about 17% of the subcutaneous exposure by AUC, with Tmax 0.63–0.75 h against 0.25–0.38 h and Cmax of 4.31–11.2 ng/mL. That is the arithmetic behind the dose gap on the two labels: 1–6 mg subcutaneous U.S. Food and Drug Administration 2025 against 10–30 mg sublingual film U.S. Food and Drug Administration 2022. It also means a sublingual product measured in two or three milligrams — the dose used in the erectile-dysfunction work Dula 2001 — is delivering a fraction of a rescue dose, which is the correct way to read the two indications as one dose-response curve rather than as two drugs.
What would have to be true, and how you would know it was not
Four predictions. The first is the cleanest endocrine test in this whole cohort, and the last two argue against the compound.
1. Prolactin should fall and growth hormone should rise, within the hour. This is not extrapolation — it is what apomorphine has been used as a probe for in neuroendocrinology for decades. Dopamine is the physiological brake on lactotrophs, so a broad-spectrum dopamine agonist Jenner 2016 should push prolactin down and, through hypothalamic D2 receptors, push growth hormone up. Draw both at baseline and again 45 to 60 minutes after a dose, matched for time of day and with no meal in between. This is a falsification test for the whole page: if prolactin does not move at a dose that makes you nauseated, the material is not what it says it is, because the emetic effect and the prolactin effect run through the same receptor family.
2. If it is being used for erectile function, the read-out is an instrument, not an impression. Score the IIEF across a defined two-week baseline before the first dose and again over a matched two-week window on it. Dula 2001 needed 296 men to separate 3 mg from placebo, which tells you the effect is real and modest; an effect of that size is exactly the kind a person cannot detect in themselves without a baseline written down in advance.
3. The prediction that cuts against it: nausea should arrive before benefit, and it should track dose steeply. The area postrema sees the drug first, so at any dose producing a central effect the emetic effect is already present. The published slope is brutal — 3.3% nausea at 3 mg and 14.1% at 4 mg Dula 2001 — and even in Parkinson’s patients pre-treated with trimethobenzamide the label still records 31% nausea and 11% vomiting U.S. Food and Drug Administration 2025. So the falsifiable claim is: there is no dose at which you get the effect and no nausea. Anyone reporting a clean, nausea-free response at a dose producing an obvious central effect is describing something other than apomorphine pharmacology.
4. Blood pressure should drop on standing, measurably, within the hour. Take lying and standing blood pressure at baseline and at 20 and 40 minutes after a dose. The label’s own numbers set the expectation: systolic orthostatic hypotension rose from 4% pre-dose to 18% post-dose, and 11% had orthostatic hypotension, hypotension and/or syncope U.S. Food and Drug Administration 2025. A postural drop is the mechanism, not a surprise — and it is why the 5-HT3 antagonist combination that produced loss of consciousness is a contraindication rather than a caution.
What nobody has tested yet
Nobody has established how a human clears this drug. The label states in plain words that the route of metabolism in humans is not known U.S. Food and Drug Administration 2025. Sulfation, N-demethylation, glucuronidation and oxidation are all candidates and they have very different genetic variability, so the reason two people respond differently to the same milligram cannot currently be investigated. A mass-balance study with a radiolabelled dose in six volunteers is a standard, decades-old experiment, and for this molecule it has never been published.
Nobody has found where the extra clearance happens. Apparent clearance of 223 L/h U.S. Food and Drug Administration 2025 exceeds hepatic blood flow, which means a meaningful share of elimination is happening outside the liver. Identifying it — plasma sulfotransferase, red cells, kidney — would be an afternoon of in-vitro work with human blood and would immediately explain the threefold range in the label’s own clearance figures.
Nobody has measured the emetic and the erectile dose-response in the same person. That ratio is the entire commercial history of this molecule, and it exists only as separate group means from separate trials. A within-subject dose escalation — 2, 3, 4 mg, with an IIEF response and a nausea visual-analog score at each step — would produce the per-person therapeutic window that decides whether anybody should use it, and it has never been run.
Nobody has used the prolactin response as a dose-finding tool. Titration of apomorphine is currently done by trial, starting at 1–2 mg and escalating U.S. Food and Drug Administration 2025, with vomiting as the feedback signal. Prolactin suppression is a single blood draw, moves within an hour, and is driven by the same receptor family as the therapeutic effect. Whether it predicts the individual motor or erectile response has never been tested, and it is the cheapest unasked question on this page.
Apomorphine — its own safety story, not its class's
The contraindication first, because it is unusual and it is lethal-sounding for a reason. Apomorphine must not be combined with 5-HT3 antagonists — ondansetron, granisetron, dolasetron, palonosetron, and alosetron — because of reports of profound hypotension and loss of consciousness when it was given with ondansetron U.S. Food and Drug Administration 2025. Note what that means practically: the antiemetic class a person is most likely to already own, and the class of the very compound sitting a few pages away in this same catalog, is the one class forbidden here. The label’s answer is trimethobenzamide 300 mg three times a day, started three days before the first dose, and generally continued no longer than two months U.S. Food and Drug Administration 2025.
The nausea numbers, with and without that premedication. In the label’s 12-week study nausea or vomiting occurred in 43% of patients on trimethobenzamide against 59% without it — premedication removes some of the problem and nowhere near all of it. Across the clinical studies, 31% had nausea and 11% vomited despite premedication U.S. Food and Drug Administration 2025. Any description of this compound that treats nausea as an occasional nuisance is not describing the published record.
The cardiovascular and neurological warnings, with the label’s own percentages. Systolic orthostatic hypotension rose from 4% pre-dose to 18% post-dose, and 11% had orthostatic hypotension, hypotension and/or syncope. Somnolence was reported in 35% of apomorphine patients and none on placebo, including sudden-onset sleep. Hallucinations in 14%. Impulse control disorders — compulsive gambling, spending, eating and hypersexuality — are a warning for every dopamine agonist and apply here. QTcF was prolonged by 10 msec (90% upper confidence interval 16 msec) U.S. Food and Drug Administration 2025.
Route-specific harm, which differs completely between the two approved products. Subcutaneous: 26% had injection-site reactions, including bruising 16%, granuloma 4% and pruritus 2% U.S. Food and Drug Administration 2025. Sublingual film: oral or pharyngeal soft-tissue swelling in 15%, oral soft-tissue pain and paraesthesia in 13%, oral mucosal erythema in 7%, and the label warns that rechallenge is not generally recommended after discontinuation, as oral reactions may recur and be more severe U.S. Food and Drug Administration 2022. That last sentence is the one to notice: it is a tissue reaction that gets worse on re-exposure, which is not how an ordinary irritation behaves.
And the risk this compound does not carry, stated because the name creates it. There is no opioid activity, no respiratory depression through an opioid mechanism, no opioid tolerance or withdrawal, and naloxone is not an antidote. The dangers here are dopaminergic and hemodynamic. Treating apomorphine as a morphine relative leads people to watch for the wrong emergency — the one that actually happens is a syncopal episode on standing, in the first hour, in someone who took an antiemetic they already had in the cupboard.
Sources read for this page
- U.S. Food and Drug Administration. APOKYN (apomorphine hydrochloride injection), for subcutaneous use - full prescribing information (NDA 021264).. FDA approved labeling, revision 2025
- U.S. Food and Drug Administration. KYNMOBI (apomorphine hydrochloride) sublingual film - full prescribing information (NDA 210875).. FDA approved labeling, revision 2022
- Jenner P. Apomorphine - pharmacological properties and clinical trials in Parkinson's disease. Parkinsonism Relat Disord 2016 · PMID 27979722
- Dewey RB Jr. A randomized, double-blind, placebo-controlled trial of subcutaneously injected apomorphine for parkinsonian off-state events. Arch Neurol 2001 · PMID 11559309
- Katzenschlager R. Apomorphine subcutaneous infusion in patients with Parkinson's disease with persistent motor fluctuations (TOLEDO): a multicentre, double-blind, randomised, placebo-controlled trial. Lancet Neurol 2018 · PMID 30055903
- Olanow CW. Apomorphine sublingual film for off episodes in Parkinson's disease: a randomised, double-blind, placebo-controlled phase 3 study. Lancet Neurol 2020 · PMID 31818699
- Dula E. Double-blind, crossover comparison of 3 mg apomorphine SL with placebo and with 4 mg apomorphine SL in male erectile dysfunction. Eur Urol 2001 · PMID 11464037
- Agbo F. Pharmacokinetics and Comparative Bioavailability of Apomorphine Sublingual Film and Subcutaneous Apomorphine Formulations in Patients with Parkinson's Disease and OFF Episodes. Neurol Ther 2021 · PMID 33991326
Apomorphine — safety, predicted from mechanism
Predicted from mechanism, not from a human safety trial. How that reasoning works →
What the mechanism predicts
Derived from the molecule, not a trial.
- This group acts directly on established CNS receptors — GABA-B (phenibut), serotonergic and histaminergic (trazodone, doxepin), beta-adrenergic (propranolol), dopaminergic (cabergoline, apomorphine). These are pharmacological drugs, not research peptides, and the predicted problems are the known ones for each receptor.
- Phenibut is the one that needs saying plainly: it is physically addictive. GABA-B agonism produces tolerance within days of regular use, and withdrawal is genuinely severe — anxiety, insomnia, tremor, and in heavy users, psychosis and seizures. It is closer to a benzodiazepine than to a nootropic in this respect, and it is sold as though it were the latter.
- Propranolol blunts the physical symptoms of adrenaline. That predicts the useful effect and also the problem — it blunts the training response and masks hypoglycemia.
- Dopamine agonists predict nausea, orthostatic hypotension and, at the doses used in Parkinson's, impulse-control problems. Cabergoline's half-life is very long, so effects persist well past a dose.
What has actually been reported
- Phenibut dependence and withdrawal are well documented in case reports and poison-center data.
- Trazodone: sedation, orthostatic hypotension, and rarely priapism — which is a medical emergency.
- Abrupt propranolol cessation causes rebound tachycardia and hypertension. Do not stop a beta-blocker suddenly.
- Cabergoline at high cumulative doses is associated with cardiac valve changes; at the low doses used for prolactin this has not been shown.
How to reduce the risk
Same mechanism as the prediction.
- For phenibut, the only reliable mitigation is frequency: occasional use does not produce dependence, regular use does. There is no dose that makes daily use safe.
- Taper anything in this group rather than stopping abruptly.
- Take the first dose of anything with orthostatic effects at home, sitting down.
What it does to your bloodwork
A fact about the assay.
- Prolactin if using cabergoline (it is usually why you are). Otherwise blood pressure and heart rate are the monitoring that matters.
Don't run this if
- You already take a sedative, a benzodiazepine, or drink regularly — the CNS depressant effects are additive and this is where respiratory depression comes from.
- You are on an antidepressant and considering trazodone — serotonergic combinations need a prescriber, not a forum.
The honest unknown
- Most of this group is well characterized for its licensed use. What is NOT characterized is the off-label use most people here are making of it, at doses and durations nobody studied.
Not medical advice. If you take prescription medication or have a diagnosed condition, check this with a pharmacist or doctor.
Apomorphine — interference & stacking
Predicted from mechanism, not from an interaction study. How mechanism-predicted claims are made →
What Apomorphine moves on your bloodwork
Expected direction, not a measured one.
- Complete Blood Count (CBC) with Differential — ↑ expected to rise
Hematocrit and hemoglobin rise — androgens stimulate erythropoiesis. This is the most reliably predictable movement of any compound in the Vault.
What to do: This is the number that decides whether you keep going. Baseline and every 3 months. Dehydration on the draw day inflates it, so hydrate normally or you will chase a false reading. - Total Testosterone — ↑ expected to rise
Expected. Trough vs peak matters enormously — the same protocol reads completely differently depending on when you drew.
What to do: Draw at the same point in the cycle every time or the trend is noise. - LH & FSH — ↓ expected to fall
Suppressed by negative feedback. This is the mechanism, not a side effect — and it is why exogenous androgen shuts down your own production.
What to do: Relevant if fertility matters to you. Worth knowing before, not after. - Estradiol, Sensitive (LC/MS-MS) — ↑ expected to rise
Aromatization converts a fraction to estradiol, and it rises with the androgen. Use the sensitive (LC-MS/MS) assay — the standard immunoassay is unreliable in men and produces numbers people then medicate.
What to do: If you are reading estradiol in a man, the assay choice matters more than the result. - SHBG (Sex Hormone-Binding Globulin) — ↓ expected to fall
Falls with androgen exposure, which raises the free fraction — so free testosterone can climb faster than total.
What to do: Read total and SHBG together; total alone understates what changed. - Lipid Panel (Cholesterol, HDL, LDL, Triglycerides) — ↓ expected to worsen
HDL falls, sometimes markedly. Oral 17-alpha-alkylated compounds do this far more aggressively than injectable esters.
What to do: Baseline and 12 weeks. ApoB is the better long-term read than LDL-C. - PSA (Total + Free + % Free) — ↑ expected to rise
Androgens can raise PSA modestly. It does not create prostate cancer that wasn't there, but it can unmask it.
What to do: Baseline before starting matters — without it, a later number has nothing to be compared against.
- How to work up to it, and when not to
- When to take it, and why that window
- Cycle length
- Time off between cycles
- Fasted or fed, and when in the day
- Coach Cam's personal notes
- Which compounds push the same lever, and why the dose adds up faster than people count
- What blunts it — the stacks that waste your money
- What compounds the risk, so a side effect arrives sooner than any one of them suggests
- Coach Cam's read on running it alongside the rest of your protocol
Everything above is free and stays free. Skool is where it becomes a plan — Apomorphine in an order, with the rest of what you're running.
Unlock in Skool — $10/mo →Bloodwork to run alongside Apomorphine
Baseline first, then again at 8–12 weeks.
| Marker | What it’s watching for |
|---|---|
| Total Testosterone | The baseline you can't reconstruct later |
| Free Testosterone | The fraction that does anything — total alone misleads |
| SHBG (Sex Hormone-Binding Globulin) | Explains a normal total sitting on top of a low free |
| Estradiol, Sensitive (LC/MS-MS) | The other half of the ratio, and the source of most symptoms |
| LH & FSH | Separates a testicular problem from a pituitary one |
The “Low T? Rule Out the Reversible Causes First” panel covers these in one order — 11 markers, $211.50 with the discount applied.
Check results you already have → · All 103 markers A–Z
Apomorphine — frequently asked questions
What is Apomorphine?
Apomorphine (Apomorphine HCl) is a hormonal & sexual research compound. Non-selective dopamine agonist acting centrally at the paraventricular nucleus — it drives erection through the brain rather than through vascular smooth muscle, which is a completely different route from a PDE5 inhibitor.
Is the full Apomorphine protocol on this page?
The reported research dose is on this page, along with how Apomorphine works and the evidence behind it. The protocol — how to work up to it, frequency, cycle length, time off, what not to stack it with and Coach Cam's notes — is inside Skool.
What is the half-life of Apomorphine?
Apomorphine has an approximate half-life of ~40 minutes, which is part of what determines how often it's dosed.
What's the evidence behind Apomorphine?
Current evidence level: Was approved in Europe as Uprima; withdrawn commercially rather than for safety. Apomorphine is offered for research purposes only and is not an approved medicine.
What Apomorphine is used for
Apomorphine appears under 1 goal in the goal router.
Related Hormonal & Sexual compounds
Where this goes next
The pages here are the frameworks. The protocols — the dosing, the order to correct things in, the week-by-week schedule and what to retest — are inside Skool.