Precision
Dutasteride
Designed to strongly inhibit scalp 5α-reductase while minimizing systemic absorption.
- 1Dutasteride inhibits both type I and type II isoenzymes for powerful suppression of scalp DHT.
- 2Anagen's proprietary delivery vehicle causes liposomes to preferentially aggregate in a follicular reservoir for localized diffusion to dermal papilla cells.
- 3At our new 1% dose, an early two-person blood check found serum dutasteride below the assay's limit of quantification.
Why we deliver through the follicle.
Dutasteride is one of the most potent DHT blockers there is, but its target sits deep inside the follicle, and taken orally it suppresses DHT across the whole body. The entire job of a topical is to put that potency at the follicle and minimize systemic absorption. That's a delivery problem, and it's the one Precision Dutasteride's vehicle is built to solve.
- 1The target is deep and local. Inside the follicle, 5α-reductase converts testosterone into DHT, and DHT acts on the dermal papilla at the base of the follicle to miniaturize it. The drug has to reach the dermal papilla, locally, deep in the follicle.
- 2Flat skin blocks the way. The stratum corneum, the skin's outer "brick-and-mortar" layer (keratin cells packed in a lipid matrix), is the rate-limiting barrier to topical drugs; intact lipid vehicles essentially can't cross it.
- 3The follicle is the shortcut. The follicle opening bypasses that barrier: the drug and its lipid vesicles funnel down the follicular canal and pool in the sebum as a long-lived "follicular reservoir": reaching depth, and lingering, in a way flat-skin diffusion can't.
- 4A localized gradient does the targeting. Concentrating the drug in the follicle builds a steep local concentration gradient. By Fick's law, diffusion flows from high to low concentration: a strong push across the thin canal wall into the dermal papilla, exactly where it's needed. Because the depot is small and local, the outward gradient is weak, so little drug spreads to the deeper dermis or the bloodstream.
That is the whole rationale for follicular targeting: the local action of dutasteride with far less of the systemic trade-off. Which is why we screened dozens of vehicles for exactly this property, and the rest of this page is the evidence the vehicle actually does it.
More than 60 delivery systems went in. One came out ahead.
A vehicle is only as good as where it puts the drug. We screened the field (liposomes, ethosomes, transfersomes, polymer nanospheres and nanocapsules, mineral carriers) for one property: routing dutasteride into the follicle.
Early Precision Dutasteride patients show no decrease in serum DHT.
If the drug truly stays local, systemic DHT should barely move. Across six early patients we monitored serum DHT (ng/dL) at baseline and follow-up. This is real-world observational monitoring (n = 6), not a randomized or controlled endpoint.
Minimal systemic DHT change, consistent with a follicle-local topical that leaves circulating hormone largely unmoved.
In skin tests, the drug concentrates in the follicle with variability between wet and dry scalp.
Targeting only matters if the drug also stays put. Ex vivo, dutasteride accumulated in the follicle while the deeper viable-skin compartment (the path toward circulation) stayed below the assay's detection limit. More dutasteride was recovered from the follicle in wet scalp conditions compared to dry.
We pushed the dose to 1%. Serum dutasteride stayed below what the assay can measure.
Two of us applied 1 mL of the 1% formulation to the scalp once daily for four days, with serum dutasteride measured by LC-MS/MS before the first dose and after the fourth. The assay's limit of quantification was 0.1 ng/mL, run with a standard curve and QCs.
All four samples came back below the assay's floor, hundreds of times under the ≈ 40 ng/mL an oral dutasteride pill puts in your blood. The damp-scalp reading ticked up and the dry one didn't, echoing the wet-beats-dry uptake we saw ex vivo (Plate 04). But both stayed below quantification, so that gap is noise. Suggestive, not proof.
To move DHT, dutasteride has to be in your blood. The 0.5 mg pill that drops serum DHT about 90% runs near 40 ng/mL, roughly 400 times our assay's floor and far above anything we measured. Even a 0.01 mg dose, the lowest in the dose-ranging studies, leaves serum dutasteride below detection. So under 0.1 ng/mL is well beneath what it takes to move circulating DHT, which is why serum DHT didn't budge in our early monitoring (Plate 03). We don't give a hard cutoff because there isn't one: dutasteride binds 5α-reductase for good, so the effect follows enzyme turnover, not a single blood level.
Four days is not steady state. So both participants kept applying for another four weeks — Participant 1 holding at 1 mL a day on a damp scalp, Participant 2 doubling to 2 mL a day on a dry one. At day 30 we drew serum again on a fresh batch. This time both samples cleared the LLOQ of 0.1 ng/mL.
Participant 1, at 1 mL a day, measured 0.157 ng/mL. Participant 2, who had doubled to 2 mL a day, measured 0.282 ng/mL. A 0.5 mg oral dutasteride capsule sits near 38 ng/mL at steady state, so the heavier of the two topical doses landed at roughly three quarters of one percent of the oral serum concentration.
Two men at two different doses gives us more than two numbers. It gives us a rate, and a rate works on every strength we make.
Every milligram you apply puts about 0.015 ng/mL into your blood.
| Formula | Daily volume | Drug applied | In your blood | Source |
|---|---|---|---|---|
| 0.03% | 1 mL/day | 0.3 mg | 0.005 ng/mL | modeled |
| 0.3% | 1 mL/day | 3 mg | 0.045 ng/mL | modeled |
| 1%Participant 1 | 1 mL/day | 10 mg | 0.157 ng/mL | measured |
| 1%Participant 2 | 2 mL/day | 20 mg | 0.282 ng/mL | measured |
| XYON 2% gelcompetitor, n = 9 | not stated | not reported | 1.34 ng/mL | measured |
| Oral capsulefor scale | one capsule | 0.5 mg | 38 ng/mL | published |
Only the two 1% rows were measured in our own participants. The 0.03% and 0.3% rows are this constant projecting from those two men, and have never been observed directly. The XYON row is their own published figure from a patent filing, where the amount applied was described only as a thin layer and never reported. The oral row is published data, shown so the scale is visible.
Participant 1 applied to a damp scalp and took up 0.0157 ng/mL per milligram. Participant 2 used a dry scalp and took up 0.0141. Those are close, within 11%. That is one person per condition, and their doses differed too, so read it as a hint and not a finding.
It rests on two people. Published dutasteride pharmacokinetics vary roughly 70% between individuals, so one person can sit well outside these numbers. A July sample on 0.3% at 2 mL came back under the assay floor, which this constant predicts at 0.089 ng/mL. That agreement rules out constants above 0.0167 and nothing tighter.
So what does that do to DHT? We did not measure it in either participant, so the honest answer is a range rather than a number. Here is what the published curve predicts, and how that compares to the way serum DHT drifts on its own.
How far these doses are expected to move serum DHT.
Every topical dose is predicted to move DHT less than it drifts on its own. Serum DHT is not a steady number. Draw blood from the same man twice with no treatment at all and the two results differ, half the time by more than 18% to 28%. All four topical predictions sit under that. The oral capsule does not, and that gap is what the product is built around.
XYON reports 1.2 to 1.5 ng/mL of dutasteride in the blood on their 2% gel, and no measurable change in DHT, in 9 men. Those two numbers are hard to hold together. In the trial GSK filed with the Japanese regulator, men at 1.51 ng/mL saw serum DHT fall 64.9%, in 65 men, p below 0.001. The curve behind every other number on this chart predicts 59% at XYON's serum dutasteride concentration. Gold standard randomized trial data, and our own model built on that data, both predict vastly more DHT suppression than XYON reported.
GSK CTD Module 2.7, submitted to Japan's PMDA for dutasteride in male pattern hair loss, Table 2.7.2.2-2 (serum dutasteride) and Table 2.7.2.2-6 (serum DHT), study ARIA2004, week 24. XYON figures from US patent application 2023/0181430 A1, Tables 9 and 11.
DHT was not measured in either participant. These are projections from a curve fitted to Clark 2004, resampled to carry its uncertainty, and our exposures sit below the lowest concentration Clark measured directly. Read the ranges, not the midpoints. Scalp DHT, the endpoint that decides whether a follicle-targeted vehicle works, has never been measured in a human on this formula. That is what the trial is for.
Dutasteride's hair-growth efficacy as a dual 5α-reductase inhibitor is well established and covered in depth elsewhere. This page is about delivery: getting that established molecule into the follicle while minimizing systemic absorption.
Targeted vehicle
The winning vehicle routes drug into the follicle: 0.64 vs ≈ 0.47 for the best alternative.
Measured · ex vivoSerum DHT unmoved
Across 6 early patients, serum DHT showed no decrease (+10.6%); stays within range.
Observed · n = 6Stays in the follicle
Drug accumulates in the follicle; the deeper systemic route stayed below detection.
Measured · ex vivoBelow quantification at 1%
At our highest dose, serum dutasteride stayed below the assay's limit of quantification, before and after.
Observed · n = 2Dial the strength
0.03% and 0.3%, plus a new 1%. A clinician dials the local dose to the plan.
ProductThree strengths, one follicle-targeting vehicle.
Choose from 0.03%, 0.3%, and 1%. A licensed clinician decides which strength is right for you.
What this page can and can't support
- Vehicle data is ex-vivo follicular targeting: a delivery measure (where the drug goes), not clinical hair growth, and not serum-DHT suppression on its own.
- The serum-DHT set is observational (n = 6), not a controlled PK or hormone study; stable DHT is the expected result for a topical, not proof of efficacy.
- The 1% systemic check is a two-person pilot: every reading sat below the assay's limit of quantification (0.1 ng/mL). It shows no measurable systemic rise at a high dose, not a guarantee of zero absorption, and a larger sample is needed to confirm it.
- 0.3% serum-DHT monitoring is pending: we report only what we've measured, and Precision Dutasteride (0.3%) hormone data is not yet available.
- Prescription product, clinician-gated. Suitability is decided by a licensed clinician. This page is treatment science, not medical advice.
