Ibogaine QTc Risk Calculator
Estimate peak QTc on ibogaine using your baseline EKG, electrolytes, age, sex, CYP2D6 status, and co-medications searched live against our drug interaction database. Identify hard stops, caution factors, and modifiable factors before booking, and walk into your medical review prepared.
What's actually happening in your body, step by step
Ibogaine and noribogaine bind to the hERG potassium channel in heart tissue, which resets the electrical cycle between heartbeats. Blocking it delays that reset, which is measurable on an EKG as a longer QT interval. This happens to some degree in nearly every patient; it's a property of the molecule, not a rare side effect in a few unlucky people.
A heart that starts with a shorter QT interval has more room to absorb that delay safely. One that's already near the upper edge of normal, whether from genetics, medication, or electrolyte imbalance, has far less margin before the added effect pushes it into a range where dangerous rhythms become statistically more likely.
Dozens of common medications (certain antidepressants, antipsychotics, antibiotics, and antiarrhythmics among them) independently prolong QT through unrelated mechanisms. Low potassium or magnesium does the same, directly, without any drug involved. None of these need to be dangerous alone; the risk comes from several landing on the same heart at the same time.
Noribogaine (ibogaine's active metabolite) is cleared almost entirely through the CYP2D6 liver enzyme. People who metabolize poorly through that pathway, or who are taking a drug that blocks it, keep higher noribogaine levels in circulation for longer, which extends how long the QT-prolonging effect lasts, not just how strong it is.
Go deeper in our safety and monitoring protocol, the full drug interaction directory, and our cardiac risk deep-dive.
What clinicians and patients ask about the QTc workup
Why does ibogaine affect the heart's electrical rhythm at all?
Ibogaine and its metabolite noribogaine bind to the cardiac hERG potassium channel, which controls how quickly heart cells reset between beats. Blocking that channel delays the reset, which shows up on an EKG as a longer QT interval. It is a pharmacological side effect of the molecule itself, not a sign that something has gone wrong with your heart beforehand. A heart that is already vulnerable, due to low electrolytes, genetic long QT, or other QT-prolonging drugs on board, tolerates that delay far worse.
This tool gives me a number. What does a treatment center actually do with it?
A calculated estimate is a conversation starter, not a clearance. A real screening visit repeats the EKG in person, pulls a full metabolic panel (potassium, magnesium, liver, kidney), and in many cases adds CYP2D6 testing or a cardiology consult before anyone commits to a dosing date. Because we're a directory and not a single clinic, we built this tool to help you walk into that conversation already knowing which of your own factors are worth asking about. It's meant to prepare you for that conversation, not replace it.
Why do some centers require a lower baseline QTc than the general cardiology guideline?
General cardiology guidelines treat roughly 450ms (men) and 470ms (women) as the upper edge of normal, with 500ms as the point where arrhythmia risk climbs sharply. Because ibogaine itself adds tens of milliseconds on top of baseline, a stricter pre-treatment ceiling gives a safety margin before that climb even starts. Protocols vary between centers, since not every center screens to the same bar, which is exactly why we built the directory filter for cardiac-protocol strength.
Which of these risk factors can I actually fix before I'm screened again?
Electrolytes are the fastest lever. Correcting low potassium or magnesium under medical supervision can shift QTc within hours, not weeks. Medication changes take longer and need a prescriber involved: tapering off a QT-prolonging drug or switching away from a CYP2D6 inhibitor plays out over days to weeks, not overnight. Genetic factors (family history of long QT, confirmed poor-metabolizer status) aren't fixable, but disclosing them changes what monitoring a center should put in place for you.
Why build this as a calculator instead of just listing which drugs are risky?
Because risk doesn't add up as a simple checklist. A mild SSRI effect and a borderline baseline QTc together can matter more than either alone, and a single moderate factor (e.g. low potassium) can be fixed in a day while a genetic one can't. Our existing drug interaction directory still lists every medication's standalone interaction category; this tool layers the actual arithmetic on top so you see how several factors compound, not just that each one individually "matters."
Does a clean result here guarantee I'll be cleared for treatment?
No, and we'd rather be blunt about that than reassuring. This estimates a population-average effect from published dosing literature, individual patients vary, and only a same-day 12-lead EKG plus a physician's in-person review can actually clear someone for dosing. Treat a favorable result here as permission to keep moving forward with real screening, not as the screening itself.
Now take this number into a real screening
Compare verified centers by how thorough their cardiac workup actually is: on-site cardiologist, continuous ECG monitoring, and IV electrolyte repletion all vary by center.
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