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Definition

DHT inhibition

Dihydrotestosterone (DHT) contributes to androgen-responsive follicular changes in susceptible individuals. This service investigates defined ways of limiting DHT production or signaling, not a single assay that establishes prevention of hair loss.

Formation of DHT

5α-reductase assays measure conversion of testosterone to DHT using a stated enzyme source or cellular system. Direct product measurement and concentration-response analysis can characterize inhibition of synthesis, with relevant isoforms and reference controls documented.

  • DHT formation relative to vehicle controls
  • IC50 values where supported by the measured response
  • Assay interference and sample compatibility checks

Response to existing DHT

Dermal papilla or other suitable androgen-responsive models can assess receptor signaling in the presence of DHT. Receptor binding, reporter activation, and downstream gene expression answer different questions and should not be treated as interchangeable. A binding affinity requires a dedicated binding experiment. Viability and proliferation measurements help identify nonspecific effects. Neither enzyme inhibition nor altered receptor signaling alone establishes clinical efficacy against androgenetic alopecia.

Applications

Separate hormone formation and signalling

5α-reductase assays measure conversion of testosterone to DHT in a specified enzyme or cellular system. Concentration-response data and appropriate controls help characterise inhibition. Relevant isoforms and direct product measurement should be documented.

Androgen-responsive cell models can instead investigate signalling in the presence of DHT. Receptor binding, reporter activity and downstream expression are distinct measurements. Include viability and interference checks before attributing a response to selective inhibition.

Results can rank candidates for subsequent follicle, delivery or human studies. Assay potency is not a safety threshold, clinical proof against androgenetic alopecia or automatic support for hair-growth advertising. Product classification and claim requirements depend on the intended market.

Exploration
Learn more about Hair Follicle & Fibre

Investigate hair follicle and fibre biology through keratin, pigment, growth and androgen-related endpoints, separately from visible human hair outcomes. Explore another Hair Follicle & Fibre page on cosmetic-labs.com.

Hair care efficacy testing

Investigate hair-fibre protection, follicle biology and scalp mechanisms using fibre analysis, cell cultures and isolated follicle models as appropriate.

Stem cell activation

Investigate identified hair follicle stem-cell responses using marker and functional assays that distinguish activation from general cell proliferation.

Growth-factor stimulation

Measure production or release of selected growth factors in hair-relevant cells to investigate follicle signalling without claiming hair regeneration.

Keratin synthesis

Measure keratin production in living follicle cells or suitable models to investigate hair development, separately from existing hair-shaft repair.

Follicular 5α-reductase

Measure follicular 5α-reductase activity and ingredient inhibition to investigate testosterone-to-DHT conversion, separately from receptor responses.

Hair growth efficacy testing

Measure growth-related responses in follicular cells or isolated follicles through shaft elongation and growth-phase endpoints before human studies.

Unwanted growth inhibition

Assess reduced growth in follicle-relevant laboratory models, interpreting growth endpoints alongside viability to distinguish inhibition from damage.

Hair Pigmentation Mechanism Studies

Investigate hair pigment biology through melanocyte and follicle models, with melanin and stress endpoints kept distinct from visible greying outcomes.

Matrix protein protection

Assess structural protein protection in hair fibres after controlled stress exposure, using protein analysis separately from living-follicle synthesis.

DHT inhibition

Investigate DHT formation or androgen-receptor responses in hair-relevant models, distinguishing hormone synthesis inhibition from downstream effects.

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