Introduction to the AGA Animal Model

Androgenetic alopecia (AGA), also known as male‑pattern baldness, is the most common form of hair loss. Its pathogenesis is closely linked to abnormalities in androgen metabolism, miniaturization of hair follicles, genetic susceptibility, and disruption of the hair follicle growth cycle. The hallmark pathological features include progressive follicular atrophy, conversion of terminal hairs to vellus hairs, shortening of the anagen phase, and a decline in hair density. Because experimental animals differ from humans in their sensitivity to androgens, researchers commonly employ testosterone‑ or dihydrotestosterone (DHT)‑induced models, human hair follicle transplantation models, and genetically engineered models. These models exhibit characteristics such as slowed hair growth, degenerative changes in hair follicles, and reduced activity of hair follicle stem cells, thereby mimicking certain aspects of the AGA disease process.

Advantages of Aniphe BioLab’s AGA Animal Model Platform Services

Aniphe BioLab has established a well‑established animal model platform for androgenetic alopecia (AGA), providing robust and reliable preclinical research support for studies on the mechanisms of hair loss and the development of hair‑growth products.

	The model system is comprehensive. It supports the establishment of multiple AGA models, including DHT‑induced, testosterone‑induced, and human hair follicle transplantation models.
	Modeling is stable and reliable. It can stably manifest the typical AGA phenotype, including delayed hair growth, miniaturization of hair follicles, and decreased hair density.
	Comprehensive evaluation metrics It encompasses hair regeneration scoring, hair density assessment, follicular morphological analysis, and molecular biomarker detection.
	Enhanced testing platform It is capable of conducting skin pathology, immunohistochemistry, hair follicle cycle analysis, and related signaling pathway studies.
	One-stop service support We offer end-to-end services, including model development, dosing regimen design, sample analysis, data interpretation, and efficacy evaluation.

Modeling cycle	3–6 weeks
Laboratory animals	C57BL/6J male mice
Positive drug	5α-reductase inhibitors: finasteride (oral), dutasteride; Local vasodilators: minoxidil (topical, a classic positive control); Antiandrogens: flutamide, spironolactone (topical or oral); Others: Platelet-rich plasma (PRP) and low-level laser therapy (LLLT) were also used as positive physical/biological controls.
Application areas	Evaluation of the anti‑hair loss efficacy and safety of novel antiandrogens and topical AR antagonists; pharmacological screening for minoxidil analogs or agents targeting new pathways to promote hair follicle growth; investigation of the underlying mechanisms governing androgen signaling and hair follicle epithelial–mesenchymal interactions; preclinical validation of sebaceous gland function modulation and oil‑control products; exploration of hair cycle regulation, maintenance of hair follicle stem cell homeostasis, and biomarkers for hair loss disorders.

Construction of an AGA animal model

01 Subcutaneous Testosterone Implant Model

Testosterone sustained-release implants or micro‑osmotic pumps are used to continuously deliver testosterone subcutaneously in experimental animals, thereby maintaining elevated circulating androgen levels over the long term. As testosterone is metabolized into dihydrotestosterone (DHT), it can progressively disrupt the hair follicle growth cycle, manifesting as a shortened anagen phase, premature catagen transition, and miniaturization of hair follicles. During model establishment, hair removal can be performed concurrently to enhance model reproducibility. This model is easy to implement and exhibits good stability, making it widely employed in studies of androgen‑mediated alopecia mechanisms and in the development of anti‑hair loss and hair‑regrowth therapies.

02 Exogenous DHT Injection Model

Subcutaneous or topical administration of dihydrotestosterone (DHT) elevates DHT levels around hair follicles, directly activating the androgen receptor signaling pathway. After several weeks of continuous treatment, AGA‑related phenotypes emerge, including slowed hair growth, a reduction in the number of hair follicles, decreased follicular diameter, and a lower proportion of follicles in the anagen phase. Because DHT is a key effector molecule in the pathogenesis of androgenetic alopecia, this model effectively recapitulates the core pathological features of AGA and is widely used for preclinical efficacy evaluation of antiandrogens, hair‑growth formulations, and hair follicle regeneration therapies.