Ibogaine, 5-MeO-DMT, and the comparative pharmacology of every medicine you might consider.

Ibogaine HCl is a purified, predictable molecule — easier to dose precisely, easier to monitor on EKG, and easier to study scientifically. Total alkaloid extracts contain variable ratios of ibogamine, tabernanthine, and ibogaline, which produce different subjective and pharmacokinetic effects. We choose HCl for medical predictability; some patients with milder needs may benefit from TA, which our medical team will discuss during admissions.

Three reasons. First, ecological: bufo alvarius (Sonoran Desert toad) populations are stressed by extraction. Second, quality control: toad-sourced material has variable 5-MeO-DMT concentrations and contains other tryptamines that complicate dose-response. Third, ethics: we don't want our medicine production to depend on animal milking. Synthetic 5-MeO-DMT is the same molecule, pharmaceutical-grade, with predictable dosing.

Yes — this is our flagship sequence. Ibogaine on day 2-3 produces the structural reset (opioid receptor reset, GDNF/BDNF expression, default mode network reorganization). After 4-7 days of stabilization and integration, 5-MeO-DMT on day 7-9 produces a non-dual peak that reinforces the integration. This is not a substitution; it is a sequenced protocol with internal logic and clinical rationale.

Each has different evidence and different mechanisms. Ketamine has the most clinical infrastructure (FDA-approved esketamine, off-label IV ketamine). Psilocybin is in advanced trials for depression. MDMA is in advanced trials for PTSD. Ibogaine has the strongest evidence specifically for addiction with co-occurring depression — the molecule is metabolized by CYP2D6 into noribogaine, a long-acting metabolite with sustained effects on serotonin reuptake and BDNF expression. For depression alone, our team will often recommend ketamine or psilocybin first; ibogaine becomes most relevant when addiction or trauma is the primary driver.

No. Iboga root bark (from Tabernanthe iboga, used ceremonially in Bwiti tradition) contains ibogaine plus 11+ other alkaloids in a chewable plant matrix. Pharmaceutical ibogaine HCl is the isolated, purified single molecule, free from cardiotoxic minor alkaloids and dosable to the milligram. Both have therapeutic value; we use HCl because medical safety requires precise dosing and predictable plasma curves.

Noribogaine is the long-acting metabolite of ibogaine, produced by CYP2D6 hydroxylation. While ibogaine itself has a half-life of ~7 hours, noribogaine persists for 28-49 hours and continues acting on serotonin reuptake and kappa-opioid receptors. The post-acute window patients describe — the 'afterglow' of clarity, calm, and reduced craving — is largely noribogaine pharmacology, not ibogaine itself. This is why CYP2D6 genotype matters: poor metabolizers produce less noribogaine and may need different protocols.