Precision Dutasteride
Patent filedPrecision Dutasteride is a topical dutasteride family available in 0.03%, 0.3%, and 1% strengths.
- Dutasteride
Starting at$79.91/ mo
Product Science · Follicular delivery
Precision
Dutasteride
Designed to strongly inhibit scalp 5α-reductase while minimizing systemic absorption.
- 01
Dutasteride inhibits both type I and type II isoenzymes for powerful suppression of scalp DHT.
- 02
Anagen's proprietary delivery vehicle causes liposomes to preferentially aggregate in a follicular reservoir for localized diffusion to dermal papilla cells.
- 03
At our new 1% dose, a two-person blood check found serum dutasteride below the assay's limit of quantification at day 4, and under 1% of the oral level at day 30.
01The strategy
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.
- 01
The 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.
- 02
Flat 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.
- 03
The 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.
- 04
A 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.
Key term
Stratum corneum. The skin's brick-and-mortar outer barrier, the rate-limiting step for anything applied to flat skin.
Key term
Follicular reservoir. The follicle canal acts as a shunt past that barrier and a slow-release depot for the drug.
Key term
Concentration gradient. By Fick's law, drug diffuses from high to low concentration; a steep local gradient drives it into the dermal papilla.
High exposure at the follicle, low exposure everywhere else.
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.
02The vehicle screen
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.
Figure ref
Plate 02. Each bar is one delivery system tested ex vivo, grouped by family and ranked. Bar length is its follicular targeting factor: how strongly it routes drug into the follicle versus the surrounding skin, at 12 h and 24 h.
Reading the plot
The tick on each bar marks the mineral-oil control at that timepoint (0.31 at 12 h, 0.24 at 24 h). A bar that passes its tick beats the simplest possible vehicle.
Note
The winning vehicle powers Precision Dutasteride; its proprietary identity and composition remain confidential.
Plate 02Ranked field · follicular targeting factor
- 12 h
- 24 h
- Mineral-oil control at that timepoint (12 h 0.31 · 24 h 0.24)
Precision Dutasteride
the winning vehicle
0.64
0.58
Best system in each family
PLGA nanospheres
NSPLGA3 · 233 nm
0.47
0.45
Multi-lamellar liposomes
0.16 mg/mL
0.44
0.24
Controls
Free DUT · serum
0.13
0.44
Mineral / CaHa microparticles
CaHa 5%
0.39
0.15
PCL nanospheres
NS11 · 628 nm
0.37
0.14
Nanoemulsions
NE-1 · 24 h only
not measured
0.35
Ethosomes
ET30
0.28
0.34
Liposomes
Transfersome
0.33
0.28
PCL nanocapsules
PCL20 · 459 nm
0.33
0.19
Vendor samples
Sample B · 24 h only
not measured
0.25
Show all 37 plotted systems by familyHide the full field
PLGA nanospheres
NSPLGA3
233 nm
0.47
0.45
NSPLGA2
103 nm
0.34
0.38
NSPLGA5
184 nm
0.33
0.27
NSPLGA4
169 nm
0.18
0.18
NSPLGA1
117 nm
0.11
0.34
Multi-lamellar liposomes
0.16 mg/mL
0.44
0.24
0.40 mg/mL
0.26
0.40
Controls
Free DUT
serum
0.13
0.44
DUT suspension
control
0.20
0.35
Mineral-oil control
reference
0.31
0.24
Mineral / CaHa microparticles
CaHa 5%
0.39
0.15
CaHa 2.5%
0.13
0.23
PCL nanospheres
NS11
628 nm
0.37
0.14
NS1
173 nm
0.30
0.33
NS15
891 nm
0.20
0.16
NS7
317 nm
0.15
0.09
Nanoemulsions24 h only
NE-1
not measured
0.35
NE-2
not measured
0.34
NE-3
not measured
0.31
NE-4
not measured
0.30
NE-5
not measured
0.29
NE-6
not measured
0.27
NE-7
not measured
0.26
NE-8
not measured
0.20
Ethosomes
ET30
0.28
0.34
ET30-EF
rotaevap.
0.27
0.28
Liposomes
Transfersome
0.33
0.28
LP PC + Chol
0.15
0.27
LP PC
0.14
0.13
PCL nanocapsules
PCL20
459 nm
0.33
0.19
PCL16
289 nm
0.19
0.13
PCL1
187 nm
0.17
0.05
Vendor samples24 h only
Sample B
not measured
0.25
Sample D
not measured
0.23
Sample A
not measured
0.15
Sample C
not measured
0.14
03Serum DHT
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.
Figure ref
Plate 03. Each pair of dots is one patient's serum DHT before starting Precision Dutasteride and at follow-up. The shaded band is a typical adult-male reference range.
Read honestly
A follicle-local topical should leave systemic DHT largely unmoved. Stable serum DHT is the expected, reassuring result, not an efficacy claim.
Plate 03Serum DHT · baseline → follow-up (n = 6)
- Baseline
- Follow-up
- Typical range (12–65 ng/dL)
Mean change+10.6% (n = 6)
Minimal systemic DHT change, consistent with a follicle-local topical that leaves circulating hormone largely unmoved.
04Stays local
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.
Figure ref
Plate 04. Two compartments after dosing ex vivo: drug recovered in the follicle, and drug reaching the deeper viable skin (the receptor compartment a stand in for what could enter circulation).
Key term
Below detection (ø). Too little drug to quantify with the assay; the receptor compartment did not register a measurable amount.
Plate 04Compartment recovery · follicle vs systemic
Recovered in the follicle
µg/cm² · higher = more drug held locally
~5
~9
≈1.8×
Dry scalp
Wet scalp
Reaching deeper skin (systemic route)
receptor compartment · the path to circulation
ø
ø
Below detectionno quantifiable drug in either condition
Dry scalp
Wet scalp
05The 1% test
We pushed the dose to 1%. At day 4, serum dutasteride was 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.
Key term
LLOQ. The lower limit of quantification: the smallest concentration the validated assay can measure reliably. Here it is 0.1 ng/mL. Signal below it is detectable, but the exact number can't be trusted.
The dose
1%. The highest strength we've made: about 33× the 0.03% Lite and roughly 3× the 0.3%. If any strength were going to show up in blood, it's this one.
Read honestly
Two people is a pilot, not a trial, and every day-4 reading sat below the assay's floor. This shows no measurable systemic rise at day 4, not proof of zero absorption.
Plate 05Serum dutasteride · 1% dose · baseline → day 4 (n = 2)
- Baseline (day 0)
- After 4 days
- Limit of quantification (0.1 ng/mL)
For scale▲ Oral 0.5 mg/day pill ≈ 40 ng/mL
≈ 400× above this axis · → ≈ 90% serum DHT suppression
≈ 400× above this axis · → ≈ 90% serum DHT suppression
Serum dutasteride (ng/mL)
Below limit of quantificationdetectable, but not reliably measurable
0.011
0.053
0.024
0.011
Participant 1damp scalp1% · 1 mL/day
Participant 2dry scalp1% · 1 mL/day
Every reading below the limit of quantification< 0.1 ng/mL
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.
But is that low enough to leave DHT alone?
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.
Plate 06Serum dutasteride · 1% dose · day 4 → day 30 (n = 2)
- Day 4 · below the floor
- Day 30 · measured
- Limit of quantification (0.1 ng/mL)
For scale▲ Oral 0.5 mg/day pill ≈ 38 ng/mL
≈ 110× above the top of this axis
≈ 110× above the top of this axis
Serum dutasteride (ng/mL)
LLOQ 0.1 ng/mL
< 0.1
0.1570.41% of oral
< 0.1
0.2820.74% of oral
Day 41 mL/day
Day 301 mL/day
Participant 1damp scalp1 mL/day
Day 41 mL/day
Day 302 mL/day
Participant 2dry scalp1 mL/day → 2 mL/day
Thirty days on the strongest formula we make0.157 & 0.282 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.
What reaches the blood
Every milligram you apply puts about 0.015 ng/mL into your blood.
mg applied per day×0.015=ng/mL in blood
| Formula | Daily volume | Drug applied | In your blood | Source |
|---|---|---|---|---|
| 0.03% | 1 mL/day · 0.3 mg | 0.3 mg | 0.005 ng/mL | modeled |
| 0.3% | 1 mL/day · 3 mg | 3 mg | 0.045 ng/mL | modeled |
| 1%Participant 1 | 1 mL/day · 10 mg | 10 mg | 0.157 ng/mL | measured |
| 1%Participant 2 | 2 mL/day · 20 mg | 20 mg | 0.282 ng/mL | measured |
| XYON 2% gelcompetitor, n = 9 | not stated · not reported | not reported | 1.34 ng/mL | measured |
| Oral capsulefor scale | one capsule · 0.5 mg | 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.
Wet scalp did not change what reached the blood
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.
Where this constant is thin
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.
Predicted, not measured
How far these doses are expected to move serum DHT.
- Best estimate
- Predicted DHT decrease range
0.03%
1 mL/day
under 1%
0 to 1
0.3%
1 mL/day
1%
0.2 to 5
1%
1 mL/day
7%
2 to 15
1%
2 mL/day
15%
7 to 24
Oral capsule
0.5 mg/day
95%
91 to 98
XYON 2% gel
1.34 ng/mL
they report no change
59%
53 to 67
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.
The one published result that does not fit
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.
Clinical context
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.
06The bottom line
What the evidence on this page adds up to
- 01 · DeliveryMeasured · ex vivo
Targeted vehicle
The winning vehicle routes drug into the follicle: 0.64 vs ≈ 0.47 for the best alternative.
- 02 · HormoneObserved · n = 6
Serum DHT unmoved
Across 6 early patients, serum DHT showed no decrease (+10.6%); stays within range.
- 03 · LocalMeasured · ex vivo
Stays in the follicle
Drug accumulates in the follicle; the deeper systemic route stayed below detection.
- 04 · SystemicObserved · n = 2
Under 1% of oral at 1%
At our highest dose, serum dutasteride was below the assay's limit of quantification at day 4 and 0.157 to 0.282 ng/mL at day 30, under 1% of an oral capsule.
- 05 · DoseProduct
Dial the strength
0.03% and 0.3%, plus a new 1%. A clinician dials the local dose to the plan.
07Choose your dose
Three strengths, one follicle-targeting vehicle.
Choose from 0.03%, 0.3%, and 1%. A licensed clinician decides which strength is right for you.
Explore
08Limitations
What this page can and can't support
01
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.
02
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.
03
The 1% systemic check is a two-person pilot: the day-4 readings sat below the assay's limit of quantification (0.1 ng/mL), and the day-30 readings (0.157 and 0.282 ng/mL, one participant at double the volume) were under 1% of an oral capsule's level. It is not a pharmacokinetic study, and a larger sample is needed to confirm it.
04
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.
05
Prescription product, clinician-gated. Suitability is decided by a licensed clinician. This page is treatment science, not medical advice.
09Sources
Every figure and claim, traced to its source
- 1Anagen. Internal systemic-exposure pilot: serum dutasteride by LC-MS/MS, Precision Dutasteride 1% (1 mL once daily × 4 days), n = 2, July 2026. All samples below the assay's limit of quantification (0.1 ng/mL). A pilot check, not a controlled PK study.
- 2Anagen. Internal systemic-exposure follow-up: serum dutasteride by LC-MS/MS in the same two participants after 30 days on Precision Dutasteride 1%, drawn 24 Aug 2026, single batch. 0.157 and 0.282 ng/mL; participant 2 had doubled to 2 mL a day. A pilot exposure check, not a pharmacokinetic study.
- 3Anagen. Internal patient observation: serum DHT, n = 6, June 2026. Real-world monitoring; not a controlled study.
- 4HairDAO / Universidade de Brasília. Vehicle screening: follicular targeting factor, ex vivo (porcine / rat skin). A delivery measure, not a clinical-efficacy endpoint.
- 5Clark RV, Hermann DJ, Cunningham GR, Wilson TH, Morrill BB, Hobbs S. Marked suppression of dihydrotestosterone in men with benign prostatic hyperplasia by dutasteride, a dual 5α-reductase inhibitor. Oral steady-state serum reference for the topical comparison. PMID 15126539
- 6GSK. Avodart 0.5 mg Summary of Product Characteristics. Dutasteride oral pharmacokinetics and pharmacodynamics: steady-state serum ≈ 40 ng/mL on 0.5 mg/day, with serum DHT reduced ≈ 90%. https://www.medicines.org.uk/emc/product/6758/smpc
- 7Gisleskog PO, Hermann D, Hammarlund-Udenaes M, Karlsson MO. The pharmacokinetic modelling of GI198745 (dutasteride). Low-dose serum dutasteride reaches the assay floor: a single 0.01 mg oral dose produced serum concentrations below the limit of detection. PMID 10073740
- 8Dutasteride clinical pharmacology: see the dutasteride hair-science page. https://anagen.xyz/treatment-science/dutasteride
