KY19382 for Health & Longevity

Evidence Review created on 10/24/2026 using AI4L / Opus 5.5

Also known as: 5,6-dichloroindirubin-3’-methoxime, KY-19382

Motivation

KY19382 is an experimental compound built in the laboratory from indirubin, a blue pigment of the indigo plant that also appears in some traditional Chinese herbal preparations. It was designed to switch on a cell-to-cell communication system that tells skin, hair follicles and cartilage to renew themselves. The interest in it rests on the idea that restoring this renewal signal in tissues where it has faded could address problems that existing treatments leave untouched.

The compound came out of a Korean university laboratory’s search through thousands of compounds and has been examined in cultured cells, in isolated tissue and in animals, in work on hair growth, wound repair and bone lengthening. It has not been tested in people for any of these uses and is not an approved medicine in any country. It is nonetheless discussed in online hair-loss communities and offered by suppliers of research chemicals.

This review sets out what the published record on KY19382 contains: what the compound is, how it is proposed to act, which effects have been observed and in which systems, what safety signals exist for it and for related substances, and how the evidence was produced.

Benefits - Risks - Protocol - Conclusion

Grokipedia

No Grokipedia article exists for KY19382.

Examine

No Examine article exists for KY19382. Examine covers supplements and nutrition topics and does not cover unapproved investigational compounds, which is the category KY19382 falls into.

ConsumerLab

No ConsumerLab article exists for KY19382. ConsumerLab tests marketed consumer supplements and foods, and KY19382 is not sold as a consumer product.

Systematic Reviews

No systematic reviews or meta-analyses for KY19382 were found on PubMed as of 10/24/2026.

Because no review of this type exists, neither side of the trade-off is represented: there is no systematic review or meta-analysis of the compound’s claimed regenerative effect, and none of its principal risk.

Mechanism of Action

Wnt/β-catenin signaling is a communication system that instructs stem cells in skin, hair follicles and cartilage to divide and rebuild tissue; β-catenin is the messenger protein that carries the instruction into the cell nucleus. CXXC5 (CXXC-type zinc finger protein 5, a gene whose protein acts as a brake on that system) binds a relay protein called Dishevelled and shuts the signal off. It accumulates in balding scalp follicles, non-healing wounds and ageing growth plates.

KY19382 was picked from 60 newly synthesized indirubin derivatives because it does two things at once: it occupies the Dishevelled site that CXXC5 needs, and it blocks GSK-3β (glycogen synthase kinase-3 beta, the enzyme that tags β-catenin for destruction). In cell-free assays the IC50 (concentration giving half the maximal inhibition) was 1.9 × 10⁻⁸ M against the CXXC5–Dishevelled interaction (binding assay) and 1 × 10⁻⁸ M against GSK-3β (enzyme-activity assay) (Choi et al., 2019, from a Yonsei group whose leader heads CK Regeon, the company developing the compound). Selectivity: it raised Wnt target genes without altering 19 marker genes of other pathways.

Two mechanistic readings compete. Its developers hold that releasing a brake restores signaling only where CXXC5 has suppressed it, avoiding forced activation and tumour risk. The long-standing opposing view is that any pharmacological Wnt activation carries that risk (Kahn, 2014).

Pharmacokinetics are from mice only: after abdominal-cavity injection, half-life 16.20 hours, bioavailability 16.74%, exposure 6,555.79 ng·h/mL (Choi et al., 2019). Tissue distribution, metabolizing enzymes and human pharmacokinetics are unreported.

Historical Context & Evolution

Indirubin, the chemical parent of KY19382, is an active constituent of Danggui Longhui Wan, a traditional Chinese preparation used for chronic myeloid leukaemia; its antileukaemic activity was the original reason chemists took an interest in the molecule. Two synthetic relatives, indirubin-3’-monoxime and 6-bromoindirubin-3’-oxime, were later characterised as inhibitors of GSK-3β and so as activators of Wnt signaling.

The second thread began with the identification of CXXC5 as a brake on the same pathway. A competing peptide that blocks the CXXC5–Dishevelled interaction stimulated hair regrowth and new follicle formation in mice (Lee et al., 2017). The Yonsei University group then showed the peptide also delayed growth-plate ageing and, seeking a small molecule to reproduce that effect, screened 2,280 library compounds, synthesized 60 indirubin derivatives from the top hits, and selected KY19382 for its combined activity against the interaction and the enzyme; its original intended use was height gain in children with growth retardation (Choi et al., 2019).

From 2021 onward the same laboratory, together with the company it founded — CK Biotech, later CK Regeon, whose chief executive is the group’s principal investigator — extended the compound to hair regrowth, wound healing, diabetes-impaired regeneration and skin cancer. Essentially the entire published record on KY19382 originates from this one academic–commercial group, a point that bears on interpretation. A sibling molecule, KY19334, carried the same approach into metabolic and neurological models. No part of this programme has yet produced a published human study of KY19382 itself.

Expected Benefits

All findings below come from cultured cells, isolated tissue or rodents. Not one of them has been tested in a living person, and the laboratory that produced nearly all of them has a commercial interest in the compound through CK Regeon.

High 🟩 🟩 🟩

No benefit reaches High: the required class of evidence — a human clinical endpoint or a validated clinical surrogate measured in trials from more than one research group — does not exist for this compound in any form.

Medium 🟩 🟩

No benefit reaches Medium either: there is no single human trial of KY19382 and no controlled observational human data on it; the entire record is cell culture, isolated tissue and rodent work.

Low 🟩

Speculative 🟨

Hair Regrowth

In mice, daily topical application produced more regrowth than minoxidil (Ryu et al., 2021) and restored regrowth blunted by diabetes (Ryu et al., 2022). Basis is animal and cell work only; no human trial exists.

New Hair Follicle Formation After Wounding

Mouse wounds treated with the compound formed more new follicles than vehicle- or minoxidil-treated wounds (Ryu et al., 2021). This regenerative response is weak in human scalp, so translation is unproven. Animal evidence only.

Faster Skin Wound Closure

Human skin cells migrated faster in culture and mouse wounds closed sooner (Yoon et al., 2023), diabetic ones too in independent work (Chen et al., 2025). Cell-culture and rodent evidence only.

Longitudinal Bone Growth ⭕️ Not Central to Health & Longevity

Daily injection lengthened shin bones in mice treated from early puberty into adulthood by delaying growth-plate ageing (Choi et al., 2019). It bears on childhood height; adult growth plates have closed. Mouse data only.

Suppression of Skin Tumour Development ⚠️ Conflicted

Curbed malignancy in human skin-cancer cells and mouse skin tumours (Lee et al., 2025); independent groups found it restored proliferation in other cancer cells (Shao et al., 2023). Cell and animal data only; net unresolved.

Benefit-Modifying Factors

No human study of KY19382 exists, so every factor below is inferred from preclinical work or from the biology of the target rather than measured in people.

Baseline CXXC5 level: The compound works by lifting a brake, so an effect is expected only where that brake is engaged. CXXC5 is reported as raised in balding scalp follicles, chronic wounds and ageing growth plates, and normal elsewhere.
Genetic variation: No pharmacogenetic work has been done. Variation in CTNNB1 (the gene for β-catenin, the messenger protein) and in Wnt-pathway regulators plausibly alters response, and variants affecting drug-metabolising enzymes would matter once a human route of administration existed, but neither has been tested.
Sex differences: Unknown. The mouse hair, wound and bone studies used male animals almost exclusively, and the one completed trial of a related transdermal candidate from the same company enrolled only men, so no sex comparison is available.
Age: The bone findings depend entirely on open growth plates and cannot apply to adults. For skin and hair, the rationale is that the restrainable signal weakens with age, which would favour older users, but this has not been demonstrated in people.
Pre-existing conditions: Diabetes impaired hair and wound regeneration in mice and the compound reversed that impairment, suggesting conditions that suppress this pathway may define where any effect is largest. Untested in humans.

Potential Risks & Side Effects

No person has knowingly been given KY19382 in a published study, so there are no reported side effects for the compound itself. Everything below is drawn from related compounds, from the botanical source of its chemical parent, or from laboratory work. Where human data are cited, they concern a different substance and are labelled as such.

High 🟥 🟥 🟥

No risk reaches High: the required class of evidence — documented adverse events in people exposed to this compound, replicated across independent research groups — cannot exist, since no human exposure has been studied.

Medium 🟥 🟥

No risk reaches Medium either: there is no single human trial, no case report and no observational dataset describing adverse events from KY19382.

Low 🟥

Liver Enzyme Elevation from Inhibiting GSK-3

KY19382 blocks GSK-3β. In a 26-week randomized trial of tideglusib, a different GSK-3 inhibitor taken by mouth, dose-dependent, fully reversible rises in transaminases (ALT and AST, liver enzymes released when liver cells are stressed) were among the commonest adverse events (Lovestone et al., 2015). Indirect: different compound and route.

Magnitude: Transaminase increases occurred in 9–16% of participants across the active arms and 3.5% on placebo; the trial reports no between-group difference or confidence interval for this comparison (Lovestone et al., 2015).

Adverse Events with Indirubin-Containing Herbal Preparations

Indigo naturalis, the botanical source of indirubin, has caused liver dysfunction, pulmonary arterial hypertension (high blood pressure in the lung arteries) and intussusception (bowel telescoping into itself) when taken by mouth for bowel inflammation (Naganuma et al., 2019). Indirect: a crude oral botanical, not a purified compound on skin.

Magnitude: Among 877 patients given the preparation, 91 had adverse events — liver dysfunction 40, pulmonary arterial hypertension 11, intussusception 10, of whom 40% needed surgery; no control group (Naganuma et al., 2019).

Speculative 🟨

Tumour Promotion Through Wnt Activation ⚠️ Conflicted

The pathway drives cancers when stuck on (Kahn, 2014); a developer mouse study found fewer chemically induced skin tumours (Lee et al., 2025). Basis is mechanistic and animal only; net unresolved.

Cell Toxicity Above the Working Concentration

Viability of cultured rat hair-follicle cells fell at 10 μM while 1 and 5 μM were tolerated (Ryu et al., 2021). Basis is cell-culture only; the concentration reached in human tissue is unknown.

Unquantified Systemic Absorption Through Skin

A micellar formulation was developed specifically to drive this fat-soluble molecule through skin (Seo et al., 2020), so topical use need not stay local. Mechanistic and formulation data only; no human absorption measurement exists.

Risk-Modifying Factors

As with benefits, none of these has been measured in people exposed to KY19382; they follow from the target biology and from the related compounds discussed above.

Genetic variation: Inherited activating changes in CTNNB1 or loss of APC (a gene whose protein marks β-catenin for destruction), the mutations that lock this pathway on in colorectal and other cancers, would plausibly compound any pathway activation. No screening approach has been studied.
Baseline biomarkers: Raised transaminases before exposure would leave less margin against the liver signal seen with other inhibitors of the same enzyme. No threshold specific to KY19382 exists, because no human exposure has been monitored.
Sex differences: None known. The rodent work used male animals almost throughout and the related company trial enrolled men only, so any sex difference in absorption, metabolism or adverse effects is simply unexamined.
Pre-existing conditions: Liver disease, a personal history of cancer, and conditions involving abnormal tissue growth are the obvious concerns given the mechanism and the class signals, though none has been studied for this compound in humans.
Age: Children and adolescents are a distinct concern, since the compound alters growth-plate maturation in young mice. At the older end of the adult range, cumulative cancer risk and reduced liver reserve are the relevant considerations.

Key Interactions & Contraindications

No human interaction or pharmacokinetic study of KY19382 has been published, and the compound has no product label. Nothing below can be called a contraindication on the evidence available; each entry is an inference from mechanism and is marked “(theoretical)”.

Lithium — caution (theoretical): Lithium inhibits GSK-3β by a separate route, so concurrent use could add to the same enzyme blockade, with possible larger liver-enzyme rises and excess tissue-growth signaling. No study has measured the combination, and no monitoring interval can be cited.
Other Wnt-pathway or GSK-3-directed agents (valproic acid, tideglusib) — avoid (theoretical): These and comparable investigational molecules act on the same node. The concern is additive pathway activation of unknown magnitude, with possible liver-enzyme rises and abnormal tissue growth; no human data describe the combination.
Drugs with liver toxicity (high-dose paracetamol, isoniazid, methotrexate, ketoconazole, itraconazole) — caution (theoretical): Each stresses the liver, the organ where the class signal appears, so combined use could raise the risk of drug-induced liver injury. No interaction study exists.
CYP3A4 substrates (cholesterol-lowering statins, ciclosporin, midazolam, oral contraceptives) — caution (theoretical): Indirubin, the chemical parent, switches on CYP3A4 (the liver enzyme that clears most oral drugs) in human liver cells (Kumagai et al., 2016), risking faster clearance and lost effect. Cell data only.
Over-the-counter products — caution (theoretical): Paracetamol and alcohol-containing preparations share the liver concern. Topical products applied to the same area could alter how much of the compound crosses the skin, a question no published study has addressed.
Supplements — caution (theoretical): Oral indigo naturalis delivers indirubin into human blood (Tang et al., 2025); it, woad and other indigo-plant preparations add parent-compound exposure, linked to liver dysfunction. Kava, concentrated green tea extract and comfrey add independent liver stress, raising liver-injury risk.
Supplements acting on the same pathway — caution (theoretical): Lithium orotate, sold without prescription, inhibits the same enzyme, with possible additive liver-enzyme rises. Berberine and curcumin modulate Wnt signaling in cell work, which could alter response unpredictably; human relevance is unestablished.
Other interventions — caution (theoretical): Microneedling, chemical peels and topical retinoids (vitamin A-derived skin drugs: tretinoin, adapalene) breach the skin barrier and would be expected to raise absorption of a compound already formulated for skin penetration (Seo et al., 2020).

Populations who should avoid KY19382:

People who are pregnant, planning pregnancy or breastfeeding — the pathway governs embryonic development and no reproductive toxicology has been published.
Children and adolescents with open growth plates — the compound measurably alters growth-plate maturation in young mice (Choi et al., 2019), an effect with no established human dose or safety margin.
People with a current or previous cancer, or an inherited syndrome of this pathway such as familial adenomatous polyposis (inherited growth of hundreds of colon polyps that turn cancerous) — the mechanistic concern is unresolved and no human safety data exist either way.
People with liver disease — the class signal falls on the liver, and no source gives a laboratory threshold for this compound, so the general category is named without a number.

No mitigating action — dose reduction, timing separation or a monitoring schedule — can be stated for any of the above, because none has been established in human use.

Risk Mitigation Strategies

The parameters below follow common practice for unapproved investigational compounds unless cited; no source gives thresholds specific to KY19382.

Non-use outside a trial: Not using an unapproved compound with no human safety data, no established dose and no formulation standard removes every risk listed above.
Medical supervision if used regardless: Involving a physician who knows the exposure allows liver monitoring and gives an informed starting point if symptoms appear. It mitigates the liver signal carried over from the GSK-3 inhibitor class.
Liver enzyme monitoring: Transaminases at baseline, 4 weeks, then every 3 months address the liver signal. Consensus criteria define drug liver injury as ALT above five times normal, or three times with bilirubin above twice normal (Aithal et al., 2011).
Limited treated surface area: Confining topical exposure to one palm-sized area (about 1% of body surface) reduces absorbed amount, which matters because the molecule was deliberately formulated for skin penetration (Seo et al., 2020). This mitigates unquantified systemic exposure.
Application away from broken or treated skin: Not applying to wounded, microneedled or recently peeled skin limits uncontrolled absorption, the same risk as above, and avoids compounding it with another active product.
Skin cancer surveillance: Skin examination of any treated area at baseline, then every 3–6 months, addresses the unresolved pathway-and-cancer concern directly, at the site of highest local exposure.

Therapeutic Protocol

No therapeutic protocol for KY19382 exists. The compound has never been dosed in a published human study, no leading practitioner uses it, no regulator has reviewed it, and no human dose, concentration, frequency or duration has been established for any purpose. What follows describes the regimens used in the published animal and laboratory work, which are reported here as experimental parameters and not as a human regimen; parameters not carrying a citation reflect common laboratory practice.

Animal hair-regrowth regimen: 300 μL of 0.5 mM solution in polyethylene glycol 400, applied to shaved mouse back skin once daily for 14 or 28 days; 0.5 mM was the most effective of the concentrations screened (Ryu et al., 2021).
Animal wound-healing regimen: 0.05 or 0.1 mM in polyethylene glycol 400, applied to the mouse wound daily until closure (Yoon et al., 2023).
Animal bone-growth regimen: 0.1 mg/kg injected into the abdominal cavity daily, for two weeks in short studies and ten weeks in the long one (Choi et al., 2019).
Laboratory cell concentrations: 1 and 5 μM were used in cell experiments as the range without measurable toxicity (Ryu et al., 2021).
Competing approaches: The peptide PTD-DBM addresses the same target and was itself studied in mice (Lee et al., 2017); approved hair-loss drugs act by unrelated mechanisms. No source frames any of these as a default.
Originating group: The regimens above come from the Yonsei University laboratory of Kang-Yell Choi and the company he heads, CK Regeon, which holds the development rights; no independent group has published a dosing study.
Half-life: 16.20 hours after injection into the abdominal cavity in mice, with bioavailability 16.74% (Choi et al., 2019). No human half-life has been measured.
Single versus split dosing: Animal work used once-daily administration throughout. Whether divided exposure would differ has not been examined in any species.
Time of day: Not studied. Animal dosing was given at a consistent daily time, which is routine laboratory practice rather than a finding about timing.
Genetic, sex and biomarker factors: None has been incorporated into any dosing scheme, because no human dosing scheme exists. The animal work used male mice almost throughout.
Age: All published dosing used young or adolescent mice, and the bone effect depends on open growth plates. No study has used aged animals, so whether older adults would respond to, or tolerate, the same exposure is unknown.
Pre-existing conditions: Diabetic mice responded to the same regimen as healthy ones in the hair and wound studies; no condition-specific adjustment has been described.

Discontinuation & Cycling

Intended duration: Unknown. No human use is established, so whether the compound would be short-course or continuous has never been determined; animal studies ran 2 to 40 days or until wound closure, with one bone study at ten weeks.
Withdrawal effects: None reported, and none looked for. No published study followed animals or people after stopping, so whether gains persist, fade or reverse is unmeasured.
Tapering: Not applicable on current evidence. No study tapered the compound, and no mechanism-based reason to taper has been proposed.
Cycling: Not addressed in any publication. Whether continuous use would exhaust the response, as the developers suggest happens with direct pathway activators (Ryu et al., 2021), has not been tested for this compound.

Sourcing and Quality

No pharmaceutical product exists: KY19382 is not manufactured as a medicine anywhere. Material offered online is sold for laboratory use, outside any pharmacopoeial standard, and carries no assurance of identity, purity or stability.
What to look for: For laboratory material, a certificate of analysis identifying the substance as 5,6-dichloroindirubin-3’-methoxime, with chromatographic purity and mass-spectrometric confirmation from a named laboratory, is the minimum documentation; none of this is verified by any third party for consumer use.
No third-party testing programme: Independent supplement testers do not cover investigational compounds, as the ConsumerLab and Examine searches above confirm. No equivalent of a supplement certification exists for this category.
Formulation matters: The published work used specific vehicles — polyethylene glycol 400 in the animal studies, and a mixed micellar system developed for skin delivery (Seo et al., 2020). Material supplied as a powder is not an equivalent preparation.
Reputable sources: No compounding pharmacy or named manufacturer supplies this compound for human use, and none can, since it is not an approved active ingredient.

Practical Considerations

Time to effect: Not established in humans. In mice, hair regrowth differences appeared over 14 to 28 days of daily application (Ryu et al., 2021) and wound differences within the first ten days (Yoon et al., 2023).
Common pitfalls: Treating rodent regrowth as a human result is the central error. Mouse hair cycles synchronously and mouse skin regenerates follicles after wounding in a way human scalp largely does not.
A second pitfall — confusing related compounds: KY19334 is a different molecule used in the metabolic, liver and Alzheimer’s work; findings for it are not findings for KY19382, and the two are frequently conflated in secondary coverage.
Regulatory status: Not an approved medicine; its developers reported in 2023 that no Wnt-targeting therapeutic was clinically available (Yoon et al., 2023), and the only registry entry is a completed phase 1 study of a related candidate (NCT05833906). Sale is as a research chemical.
Cost and accessibility: Available only through laboratory-chemical suppliers in milligram quantities. There is no clinical supply, no insurance pathway and no route to obtain pharmaceutical-grade material.

Interaction with Foundational Habits

Sleep: No direct interaction is known or plausible on the published mechanism; the pathway has no established role in sleep regulation. Indirectly, the liver signal carried over from related compounds would be aggravated by the alcohol intake that often accompanies disturbed sleep.
Nutrition: No direct interaction has been studied. Indirectly, indigo-plant preparations in some traditional diets and supplements supply the same chemical parent, so dietary overlap is worth noting. Alcohol adds independent liver stress alongside a class liver signal.
Exercise: None established, direct or indirect. No published study examined whether physical activity alters response, and the compound has no known effect on muscle adaptation that would argue for timing around training sessions.
Stress management: No direct interaction. The mechanism has no established link to cortisol or the stress response, and chronic stress has its own documented effects on hair cycling that are independent of anything this compound has been shown to do.

Monitoring Protocol & Defining Success

Because no human use of KY19382 is established, no validated monitoring protocol exists. What can be specified is narrow: the only laboratory concern with any human evidence behind it is liver enzyme elevation, carried over from a different inhibitor of the same enzyme. Before any exposure, a liver panel establishes an individual baseline, without which a later value cannot be interpreted. Photographic documentation of the treated area, under fixed lighting and distance, gives the only objective record of local change, since no biomarker tracks the intended effect. Ongoing monitoring has no evidence-based cadence; common practice for an unmonitored liver signal would be repeat liver enzymes at 4 weeks, then every 3 months while exposure continues, with earlier testing if symptoms appear. Success is undefined, no outcome target having been established in people.

Biomarker	Optimal Functional Range	Why Measure It?	Context/Notes
ALT	7–55 U/L (standard reference range)	Safety check; the enzyme that rises first in the liver signal seen with other GSK-3 inhibitors	ALT is alanine aminotransferase, an enzyme released from liver cells when they are injured. U/L means units per litre. Conventional laboratory reference range; no source gives an optimal functional range specific to this compound. Non-fasting sampling is acceptable
AST	8–48 U/L (standard reference range)	Safety check; paired with ALT to distinguish liver from muscle as the source of a rise	AST is aspartate aminotransferase, found in liver and also in muscle and heart. Conventional laboratory reference range. Strenuous exercise in the preceding days can raise it independently of the liver
Total bilirubin	0.1–1.2 mg/dL (standard reference range)	Safety check; a rise alongside raised enzymes marks impaired liver function rather than enzyme leak alone	Bilirubin is the yellow pigment the liver clears from the blood. Conventional laboratory reference range. Best drawn with the enzymes above in a single liver panel; fasting is not required

Qualitative markers worth tracking alongside the laboratory values:

Local skin reaction at the application site — redness, itching, swelling or blistering
Any new or changing skin lesion in a treated area, the local marker of the unresolved cancer concern
Fatigue, nausea, loss of appetite, dark urine or yellowing of the eyes, all of which point to the liver
Hair density and shedding, recorded photographically rather than by impression

Emerging Research

Only registered trial of a related candidate: NCT05833906, a phase 1 study of CKR-051 applied to the skin of 52 healthy men by sponsor CK Regeon, completed 8 January 2024 with no results posted. The registry does not state which molecule CKR-051 is.
What that trial would change: Posted results showing acceptable skin and systemic tolerance would, if CKR-051 were confirmed as this compound, give the first human safety anchor. A null or adverse outcome would undercut the safety case built entirely on rodents.
Independent replication is the pivotal gap: An independent Chinese group has reported CXXC5-blockade diabetic wound findings using the compound (Chen et al., 2025); other outside groups have used it only as a laboratory tool. Further independent work would test whether effects survive outside an interested group.
Cancer question remains open: The developers report tumour suppression in skin-cancer models (Lee et al., 2025); independent groups using KY19382 as a laboratory Wnt activator found it restored pancreatic and lung cancer-cell proliferation (Shao et al., 2023; Li et al., 2025). Independent carcinogenicity testing would settle the concern raised by Kahn, 2014.
Human follicle neogenesis may not translate: Human scalp lacks the immune cells that drive new follicle formation in wounded mice (Lee, 2025). Work resolving this would determine whether the compound’s most distinctive claimed effect is achievable in people at all.
Sibling compound as a read-across: KY19334 has been taken into metabolic, liver and Alzheimer’s models (Seo et al., 2022; Yoon et al., 2023). Human data on it would inform, without settling, the safety of the shared mechanism.

Conclusion

KY19382 is a laboratory-made relative of a plant pigment, built to release a brake on the signal that tells skin, hair follicles and cartilage to rebuild themselves. Its laboratory record is consistent: in cultured cells, in isolated tissue and in mice, it promotes hair regrowth, the formation of new follicles after wounding, faster wound closure and bone lengthening in young animals.

That record stops where human evidence would begin. No person has knowingly received this compound in a published study. There is no established dose, no approved product, no regulatory review and no safety information from human exposure. Nearly all of the published work comes from a single university laboratory and the company its lead scientist heads, which holds the development rights — a concentration of interest that weighs on how the findings are read.

The known hazards are correspondingly unmeasured. Liver enzyme increases have been documented with a different drug acting on the same enzyme, and the plant source of the compound’s chemical parent has caused liver, lung and bowel problems when taken by mouth. Whether either applies here is unknown. The long-running question of whether switching this signal on can encourage tumours is unresolved, with reassuring animal findings on one side and unresolved theory on the other.

KY19382 therefore remains an early laboratory compound: consistent in animals, untested in people.

Top - Benefits - Risks - Protocol

KY19382 for Health & Longevity

Motivation

Recommended Reading

Grokipedia

Examine

ConsumerLab

Systematic Reviews

Mechanism of Action

Historical Context & Evolution

Expected Benefits

High 🟩 🟩 🟩

Medium 🟩 🟩

Low 🟩

Speculative 🟨

Hair Regrowth

New Hair Follicle Formation After Wounding

Faster Skin Wound Closure

Longitudinal Bone Growth ⭕️ Not Central to Health & Longevity

Suppression of Skin Tumour Development ⚠️ Conflicted

Benefit-Modifying Factors

Potential Risks & Side Effects

High 🟥 🟥 🟥

Medium 🟥 🟥

Low 🟥

Liver Enzyme Elevation from Inhibiting GSK-3

Adverse Events with Indirubin-Containing Herbal Preparations

Speculative 🟨

Tumour Promotion Through Wnt Activation ⚠️ Conflicted

Cell Toxicity Above the Working Concentration

Unquantified Systemic Absorption Through Skin

Risk-Modifying Factors

Key Interactions & Contraindications

Risk Mitigation Strategies

Therapeutic Protocol

Discontinuation & Cycling

Sourcing and Quality

Practical Considerations

Interaction with Foundational Habits

Monitoring Protocol & Defining Success

Emerging Research

Conclusion