Psilocybin vs psilocin: what's the difference?

The short answer

Psilocybin is a prodrug: once it's swallowed, the body quickly strips off its phosphate group and turns it into psilocin, the compound that acts on the brain's 5-HT2A serotonin receptors.^{1, 2} Because the phosphate adds weight, psilocybin can yield at most 0.719 times its own mass as psilocin, the ratio of the two molar masses listed in PubChem, and that is the factor in Oregon's and Colorado's "total psilocin" formulas.^{3, 4, 5}

How does psilocybin become psilocin?

The two molecules are identical except at one spot. Psilocybin carries a phosphate group at the 4-position of its indole ring; psilocin has a plain hydroxyl (OH) group there instead.³ Removing that phosphate (dephosphorylation) turns one into the other.

In the body that step is fast. A 2025 systematic review of 19 publications, covering 12 clinical datasets, concluded that psilocybin "acts as a pro-drug and is rapidly absorbed and transformed to psilocin after oral administration".¹ In a pharmacokinetic study of 12 healthy adults, researchers found no intact psilocybin at all in participants' plasma or urine.⁶ Psilocin then produces the psychedelic effects by acting at the 5-HT2A receptor.²

The mushroom runs the same reaction on itself when its tissue is damaged, the first step of the bruising described below.⁷

So when a lab report lists psilocybin and psilocin side by side, it isn't listing two different drugs. It's listing the same active compound in two forms: the part that hasn't been converted yet and the part that already has.

Where does the 0.719 on lab reports come from?

Psilocybin is the heavier molecule because of its phosphate group. PubChem gives molar masses of 284.25 for psilocybin and 204.27 for psilocin, both in grams per mole.³ Divide the second by the first and you get 0.7186, rounded to 0.719. If every psilocybin molecule in a sample lost its phosphate, the psilocin produced would weigh at most 71.9% as much as the psilocybin it came from. Running the conversion the other way gives about 1.39.

Regulators use the same factor. Oregon defines "total potential psilocin" as psilocin plus 0.719 times psilocybin, which its rules call "the maximum theoretical concentration of psilocin in the sample".⁴ Colorado's "Total Psilocin" uses the same arithmetic.⁵ Because some products are labeled in psilocin terms and others in psilocybin terms, the same powder can carry different milligram figures. Our guide to what the mg on a capsule label means works through one sample read several ways.

Why do psilocybin mushrooms bruise blue?

Psilocin's free hydroxyl group makes it easy to oxidize. Psilocybin's phosphate sits on that same spot and shields it.⁷

A 2020 study in Psilocybe cubensis worked out the sequence. When the mushroom is injured, a phosphatase enzyme called PsiP removes psilocybin's phosphate to give psilocin, and a laccase enzyme called PsiL then oxidizes the psilocin. The oxidized units join into chains, mostly of 3 to 13 psilocin units, and that mixture is the blue color. The authors wrote that their results imply psilocybin's phosphate "serves a reversible protective function".⁷

The same fragility shows up in the lab. In a 1982 study, mushroom extracts kept at room temperature "within six months lost all psilocin and some psilocybin".⁸ So a psilocin figure describes a sample on the day it was tested, not the mushroom as it was picked.

Does stronger bluing mean stronger mushrooms?

No, according to the studies that checked. Beug and Bigwood measured 20 Pacific Northwest species and wrote: "we could find no correlation between degree of bluing and either psilocybin or psilocin levels".⁸ A 2026 study of six species reported that visual bluing after freezing "does not necessarily correlate with psilocin levels".⁹

The chemistry explains why. Blue pigment is psilocin that has already been oxidized, so a deeply bruised mushroom shows where conversion and breakdown happened, not how much active compound is left. Meanwhile potency differs for reasons color doesn't show: in Beug and Bigwood's data, psilocybin and psilocin levels within a single species varied by "a factor of two to more than a factor of six" between collections.⁸ The published potency measurements collect those ranges.

What are baeocystin, norbaeocystin, aeruginascin and norpsilocin?

Some lab reports list psilocybin's close chemical relatives too.

• Baeocystin is psilocybin with one fewer methyl group on its nitrogen (4-phosphoryloxy-N-methyltryptamine). It was first described in 1968 from Psilocybe baeocystis, together with norbaeocystin.¹⁰
• Norbaeocystin (4-phosphoryloxytryptamine) has no methyl groups on that nitrogen.^{10, 3}
• Aeruginascin has three, making it a trimethylammonium analogue of psilocybin. Its structure was reported in 2006 from the mushroom Inocybe aeruginascens.¹¹
• Norpsilocin (4-hydroxy-N-methyltryptamine) stands to baeocystin as psilocin stands to psilocybin: it's the form without the phosphate. It was first reported as a natural product of P. cubensis in 2017, and the authors suggested it is the active compound released from baeocystin.¹²

The first three carry a phosphate, like psilocybin. In a 2024 study, baeocystin, norbaeocystin and aeruginascin were dephosphorylated by alkaline phosphatase in vitro at nearly the same rate as psilocybin, yet only psilocybin produced head twitches in rats, a behavior researchers use as a marker in psychedelic studies.¹³ The studies we found don't establish what these relatives do in people.

Whether they're counted depends on the lab and the rules. Colorado requires labs to test for psilocybin, psilocin, baeocystin, aeruginascin and norbaeocystin, but its "Total Psilocin" figure uses only psilocybin and psilocin.⁵ Each compound has an entry in our glossary.

How does the body clear psilocin?

Free psilocin doesn't linger. Three routes break it down:

• Glucuronidation. Enzymes called UGTs attach glucuronic acid to psilocin, making psilocin-O-glucuronide, which the kidneys can excrete. Of the 19 human UGT enzymes tested in a 2010 study, UGT1A10 had the highest activity and likely acts in the small intestine, while UGT1A9 is "likely the main contributor" once psilocin has been absorbed.¹⁴ In plasma, conjugated psilocin runs about four times higher than free psilocin.²
• Monoamine oxidase A (MAO-A). This enzyme turns psilocin into 4-HIA, which other enzymes convert to 4-HIAA. MAO-A made only minimal amounts in lab tests,² but a 2025 review of the clinical data concluded that psilocin "is mainly transformed to 4-hydroxyindole-3-acetic acid [4-HIAA] and in less amounts to conjugated psilocin", with a significant portion likely converted before it reaches the bloodstream.¹
• Liver CYP enzymes. Of eight CYP enzymes tested in vitro, only CYP2D6 and CYP3A4 showed relevant activity against psilocin, and CYP2D6 genotype didn't change psilocin blood levels in the people studied.²

Across published studies, the average elimination half-life of free psilocin ranged from 1.23 to 4.72 hours, and only 1.5% to 3.4% of a dose left the body in urine as psilocin itself.¹

Thomann and colleagues expected glucuronidation to stay the predominant route and called MAO inhibition "potentially less important" for psilocin levels;² the 2025 review points more toward 4-HIAA, so this isn't settled.¹ Neither finding makes MAO inhibitors safe to combine: our interaction reference covers the MAOI, lithium and antidepressant evidence.