SW033291 is a small-molecule inhibitor of 15-hydroxyprostaglandin dehydrogenase (15-PGDH) that produced a 5-fold increase in hair growth in mouse wound healing models. This compound represents a new class of potential hair loss treatments that work by raising prostaglandin E2 (PGE2) levels in the scalp rather than blocking DHT or stimulating blood flow.
No 15-PGDH inhibitor has entered human hair loss trials yet. But the preclinical data is strong enough that myhairline.ai is preparing its tracking protocol to accommodate these compounds as soon as they reach clinical testing.
The Prostaglandin Connection to Hair Growth
Hair follicle biology is regulated in part by prostaglandins, a family of signaling molecules produced locally in skin tissue. Two prostaglandins are central to the hair loss story.
PGD2 suppresses hair growth. Research published in Science Translational Medicine found elevated PGD2 levels in bald scalp tissue compared to haired scalp in men with androgenetic alopecia. PGD2 binds to the GPR44 receptor and inhibits hair follicle growth.
PGE2 promotes hair growth. PGE2 activates Wnt signaling in hair follicle stem cells, pushing resting follicles into the active growth phase (anagen). Higher PGE2 levels correlate with thicker, faster-growing hair in both animal and human tissue studies.
The ratio between PGD2 and PGE2 appears to determine whether a follicle grows or miniaturizes. Current treatments like finasteride and minoxidil do not directly target this prostaglandin balance.
| Prostaglandin | Effect on Hair | Levels in Bald Scalp | Current Drug Targeting |
|---|---|---|---|
| PGD2 | Suppresses growth | Elevated (3x higher) | None approved |
| PGE2 | Promotes growth | Reduced | None approved |
| PGF2-alpha | May promote growth | Normal | Latanoprost (eyelash only) |
What 15-PGDH Does and Why Inhibiting It Matters
15-PGDH is the primary enzyme responsible for breaking down PGE2 in tissue. It converts active PGE2 into inactive 15-keto-PGE2, effectively removing the growth signal from the local environment.
In healthy scalp tissue, PGE2 production and degradation stay in balance. In androgenetic alopecia, DHT exposure appears to upregulate 15-PGDH activity, causing PGE2 levels to drop while PGD2 levels remain elevated. The result is a prostaglandin environment that favors follicle miniaturization.
Blocking 15-PGDH with a compound like SW033291 prevents PGE2 breakdown. Local PGE2 accumulates, and the prostaglandin balance shifts back toward growth-promoting conditions.
This mechanism is distinct from every approved hair loss treatment:
- Finasteride blocks the conversion of testosterone to DHT (80-90% halt further loss, 65% experience regrowth)
- Minoxidil increases blood flow and opens potassium channels (40-60% moderate regrowth)
- 15-PGDH inhibitors raise PGE2 to directly activate follicle stem cells (preclinical only)
SW033291: The Lead Compound
SW033291 was developed at the University of Texas Southwestern Medical Center as a tool compound to study 15-PGDH inhibition. It was not originally designed for hair loss. Researchers studying tissue regeneration discovered that SW033291 treatment in mice produced rapid tissue repair in multiple organs, including skin.
Key Preclinical Findings
The hair-related findings from SW033291 research include several notable results.
Wound healing models showed a 5-fold increase in hair growth in treated areas compared to controls. Hair follicles in treated zones entered anagen faster and produced thicker shafts.
Topical application studies demonstrated that SW033291 applied directly to mouse skin increased local PGE2 levels within hours and stimulated visible hair growth within two weeks.
Genetic knockout studies confirmed the mechanism. Mice genetically engineered to lack 15-PGDH showed elevated baseline PGE2 levels and enhanced hair cycling without any drug treatment.
| Study Type | Model | Hair Growth Result | PGE2 Increase |
|---|---|---|---|
| Systemic SW033291 | Mouse wound healing | 5x increase | 2-3x tissue levels |
| Topical SW033291 | Mouse skin | Accelerated anagen entry | 2x local levels |
| 15-PGDH knockout | Genetic mouse model | Enhanced hair cycling | Baseline elevated |
| 15-PGDH overexpression | Genetic mouse model | Reduced hair growth | Baseline depleted |
Limitations of Animal Data
Mouse hair biology differs from human hair biology in important ways. Mice cycle their hair synchronously (all follicles enter anagen together), while human scalp hair cycles asynchronously (individual follicles operate independently). A treatment that forces synchronized anagen in mice may not produce the same visible density increase in humans.
Additionally, the 5-fold growth increase was measured in wound healing contexts where tissue regeneration pathways are already activated. The effect in intact, non-wounded scalp may be smaller.
The Pipeline: From SW033291 to Human Treatments
SW033291 itself is unlikely to become a marketed hair loss drug. It was designed as a research tool and has pharmacokinetic properties (how the body absorbs, distributes, and eliminates it) that may not be suitable for chronic use.
However, several pharmaceutical companies and biotech startups are developing next-generation 15-PGDH inhibitors optimized for clinical use. The expected development timeline looks like this:
| Phase | Timeline | What Happens |
|---|---|---|
| Lead optimization | 2024-2025 | Drug candidates refined for safety and delivery |
| Phase 1 (safety) | 2026-2027 | First human dosing, safety and pharmacokinetics |
| Phase 2 (efficacy) | 2028-2029 | Controlled trials in hair loss patients |
| Phase 3 (confirmation) | 2030-2031 | Large-scale trials for regulatory approval |
| Market availability | 2032+ | If all phases succeed |
Topical formulations are expected to reach clinical testing first. A topical 15-PGDH inhibitor applied directly to the scalp would limit systemic exposure and reduce the risk of off-target PGE2 elevation in other tissues.
Why This Matters for Hair Loss Tracking
The arrival of 15-PGDH inhibitors in human trials will create a need for precise, longitudinal density tracking that current clinical trial photography cannot match.
Trial Participants Need Personal Data
Clinical trials measure group averages. A participant might respond dramatically to treatment but never see their individual data because the trial reports aggregate results. myhairline.ai allows trial participants to track their own density response independently, creating a personal record that supplements the trial's official measurements.
Early Adopters Need Baseline Documentation
When 15-PGDH inhibitors become available (whether through trials, off-label use, or eventual approval), the people who start tracking their density now will have years of baseline data. That baseline makes it possible to detect small density changes that would be invisible without historical comparison.
Combination Protocols Need Multi-Variable Tracking
15-PGDH inhibitors are likely to be used alongside existing treatments rather than replacing them. A patient might combine finasteride (DHT reduction), minoxidil (blood flow), and a 15-PGDH inhibitor (PGE2 elevation). Tracking the density response to each addition and removal requires a system that logs multiple treatment variables over time.
How myhairline.ai Will Track 15-PGDH Inhibitor Protocols
The myhairline.ai platform is built to accommodate new treatments as they emerge. The tracking workflow for 15-PGDH inhibitors will follow this structure.
Step 1: Establish a Pre-Treatment Baseline
Before starting any 15-PGDH inhibitor, capture density readings across all scalp zones. The AI generates a heatmap of current density that becomes the comparison point for all future measurements.
For users already tracking with myhairline.ai, this baseline may already exist. Years of accumulated data provide a more reliable reference than a single pre-treatment snapshot.
Step 2: Log the Treatment Protocol
Record the specific compound, dosage, application method (topical vs. oral), and frequency. If the treatment is part of a clinical trial, log the trial identifier and any known dosing schedule.
Step 3: Track Density at Regular Intervals
Take density readings every 2-4 weeks during treatment. The AI compares each reading against the pre-treatment baseline and against the most recent previous reading, producing both a cumulative change metric and a rate-of-change metric.
Step 4: Correlate With Other Variables
If you are also taking finasteride, minoxidil, PRP, or other treatments, the tracking system logs all variables simultaneously. When density changes occur, the timeline view shows which treatments were active at each point.
Comparing 15-PGDH Inhibitors to Current Treatments
The following table puts 15-PGDH inhibitors in context alongside treatments with established clinical data.
| Treatment | Mechanism | Efficacy | Status |
|---|---|---|---|
| Finasteride 1mg | DHT reduction | 80-90% halt loss, 65% regrowth | FDA approved |
| Minoxidil 5% | Vasodilation, potassium channels | 40-60% moderate regrowth | FDA approved |
| PRP | Growth factor concentration | 30-40% density increase | Clinical evidence, not FDA approved |
| Dutasteride 0.5mg | Stronger DHT reduction | Superior to finasteride | Off-label for hair loss |
| 15-PGDH inhibitors | PGE2 elevation | 5x growth in mice (no human data) | Preclinical |
The critical distinction is that 15-PGDH inhibitors target a completely different pathway. This means they could potentially be additive with every existing treatment. A patient already at maximum benefit from finasteride and minoxidil might see further gains from PGE2 elevation.
What to Do Now
If you are interested in 15-PGDH inhibitor research and want to be prepared when these treatments reach human testing, the most valuable action is to start building your density tracking baseline today.
Every month of tracking data you accumulate now becomes part of your historical record. When a 15-PGDH inhibitor eventually becomes available to you, whether through a clinical trial or later through prescription, you will have documentation that no one starting fresh can match.
Start your baseline density tracking at myhairline.ai/analyze. The analysis is free, runs in your browser, and requires no account or download.
You can also read more about PGD2 antagonist hair research and future hair loss tracking technology to understand the broader prostaglandin research landscape.
Medical disclaimer: This article discusses preclinical research compounds that have not been tested in humans for hair loss. SW033291 is a research tool compound not available for clinical use. Do not attempt to obtain or self-administer research chemicals. Always consult a licensed dermatologist before starting any hair loss treatment. myhairline.ai provides tracking and analysis tools and does not prescribe or recommend specific treatments.