After applying the product for 56 days on non-sensitive skin (61%) and sensitive skin (39%), no increase in the number of comedones was observed. The product can be labeled as non-comedogenic. The dermatologist concluded the product demonstrated very good skin tolerance.

Hair loss is medically defined as the partial or complete loss of hair from areas where it normally grows, most commonly the scalp. It encompasses a spectrum of disorders, including non-scarring types like androgenetic alopecia (pattern hair loss) and alopecia areata, as well as scarring forms. Causes range from genetic predisposition and hormonal changes to autoimmune mechanisms, environmental triggers, medications, and stress. Hair loss can be temporary or permanent, and its impact extends beyond physical appearance, often affecting psychological well-being and quality of life. (1)

Hair loss is a widespread condition affecting both men and women globally, with prevalence and patterns varying by age, sex, and underlying causes (2). By age 70, up to 80% of men and about 50% of women experience some degree of hair loss, with incidence increasing steadily with age (2,3). In men, hair loss often begins earlier and is typically more severe, presenting as thinning at the crown and temples, while in women, it tends to occur later—often after menopause—and is characterized by diffuse thinning, usually with preservation of the frontal hairline (4). The causes of hair loss are multifactorial, involving genetic predisposition, hormonal influences, environmental factors, and aging. While androgen-driven mechanisms are central, especially in men, other pathways and triggers also contribute, particularly in women (5).

Furthermore, hair loss can cause significant psychological and social distress, including anxiety, depression, low self-esteem, and social withdrawal. These impacts are seen across all types of hair loss and can affect daily functioning, work productivity, and quality of life (6). The severity of distress often increases with more extensive hair loss, but even mild cases can lead to emotional burden and stigma.

The hair follicle is a complex structure located within the dermis (Figure 1), responsible for the production and renewal of the hair shaft. It comprises multiple components with specific and coordinated functions (7,8). The hair shaft, visible at the skin surface, is composed of keratin and subdivided into the medulla, cortex, and cuticle, which respectively ensure internal structure, mechanical strength, and external protection of the hair. At the base of the follicle, the hair bulb houses the hair matrix, a zone of intense cellular proliferation where cells differentiate to form the hair shaft and the inner root sheath (9). The hair papilla, located centrally within the bulb, plays a key role by secreting growth factors that regulate the hair cycle. Surrounding the shaft, the inner root sheath guides the hair upward toward the surface, while the outer root sheath provides structural support and contains stem cells essential for follicular regeneration. The bulge, located at the junction with the epidermis, serves as a reservoir of hair follicle stem cells (HFSCs), which are activated at the onset of each new cycle (10). The sebaceous gland, connected to the follicle, secretes sebum to lubricate and protect the hair. Finally, the arrector pili muscle, attached to the bulge, induces piloerection and may influence signaling between follicular compartments (11,12). Together, these elements ensure the growth, pigmentation, protection, and renewal of the hair throughout its biological cycle.

The hair growth cycle is a dynamic and tightly regulated biological process involving the continuous regeneration of hair follicles. It comprises three main phases (Figure 2).

Oxidative stress: Oxidative stress results from an imbalance between reactive oxygen species (ROS) and antioxidants. Elevated ROS can damage hair follicle cells, disrupt the hair growth cycle, and induce premature follicle aging and apoptosis (27). This process is implicated in both androgenetic alopecia and alopecia areata, with evidence showing increased oxidative markers and reduced antioxidant activity in affected individuals (28). Oxidative stress also amplifies inflammation, creating a cycle that further damages hair follicles.

Hormonal issues: Hormones play a central role in hair growth regulation. Androgens (especially dihydrotestosterone, DHT) promote follicle miniaturization, while estrogen supports hair maintenance (29,30). Imbalances (such as increased androgens, decreased estrogen—notably during menopause—or thyroid dysfunction) can disrupt the hair cycle and lead to hair loss (31). Stress hormones (cortisol, ACTH) can also trigger early transition of hair follicles into the resting phase, contributing to diffuse hair loss (32).

Inflammation: Chronic inflammation is a key driver in several types of hair loss, including androgenetic alopecia, alopecia areata, and scarring alopecia. Inflammatory infiltrates and cytokine imbalances (e.g., IL-1, IL-6, TNF-α, IFN-γ) target hair follicles, leading to their destruction or dysfunction (33). Inflammation is often exacerbated by oxidative stress and can be influenced by dietary and lifestyle factors (34).

Genetic predisposition: Genetic susceptibility plays a fundamental role in determining individual vulnerability to hair loss. Variants affecting androgen receptor sensitivity, immune regulation, oxidative stress response, and follicular stem cell resilience contribute to the onset and severity of several alopecia types. In androgenetic alopecia, genetic factors largely dictate follicular sensitivity to DHT, while in alopecia areata, they influence autoimmune reactivity. Genetic predisposition also modulates how individuals respond to environmental triggers, explaining inter-individual variability in hair loss patterns (35,36).

UV Radiation: UV exposure causes oxidative stress, DNA damage, and inflammation in hair follicles, leading to structural damage, premature hair cycle changes, and hair follicle miniaturization. Both UVA and UVB can induce hair shaft thinning, pigment loss, and reduced stem cell populations, accelerating hair aging and loss (37).

Pollution: Airborne pollutants (particulate matter, heavy metals, PAHs) accumulate on the scalp and hair, generating ROS that damage hair fibers and follicles. Pollution is linked to increased hair fragility, scalp inflammation, and conditions like seborrheic scalpitis and folliculitis, which can mimic or exacerbate androgenetic alopecia. Pollution and UV exposure together amplify hair fiber degradation (38,39).

Chemical treatments and heat: Frequent use of hair dyes, straighteners, and perms can disrupt the hair shaft’s structure, alter amino acid composition, and cause scalp inflammation (40). These treatments are associated with increased hair breakage, shaft damage, and sometimes hair loss, especially with repeated or improper use (40,41). In addition, heat (particularly from straighteners, curling irons, and blow-dryers) also degrades the cuticle, making it more porous, brittle, and prone to breakage. Over time, this cumulative damage can reduce overall hair density (42).

Nutritional deficiencies: Deficiencies in vitamins (A, B, C, D, E), minerals (iron, zinc, selenium), proteins, and essential fatty acids impair hair follicle function and immune defense, leading to non-scarring alopecia and telogen effluvium. Correction of deficiencies can improve hair growth, but supplementation without deficiency is not always beneficial and may carry risks (43–45).

Androgenetic Alopecia: The most prevalent form of hair loss, affecting approximately 40% of men and up to 20% of women around the age of 40, with steadily increasing prevalence with age. This condition results from a genetic predisposition combined with the action of androgenic hormones, particularly dihydrotestosterone (DHT). Hair follicles located on the vertex of the scalp are especially sensitive to this hormone, leading to their progressive miniaturization: hair becomes thinner, shorter, and eventually disappears. In men, this typically manifests as crown-pattern baldness, whereas in women, hair loss tends to be more diffuse and rarely complete (46,47).

Alopecia Areata: An autoimmune disorder affecting approximately 1–2% of the general population, with onset frequently occurring before the age of 30. It is characterized by the sudden appearance of well-demarcated patches of hair loss. This form of alopecia results from an immune system dysfunction in which T lymphocytes target hair follicles as if they were foreign bodies. The exact etiology remains poorly understood, but genetic, environmental (such as stress or viral infections), and immunological factors are implicated (48,49).

Telogen Effluvium: A form of diffuse and generally temporary hair loss caused by a disruption of the hair cycle. It occurs when a significant number of hair follicles prematurely enter the telogen phase, leading to sudden and massive shedding approximately two to three months after a triggering event. Common causes include severe psychological stress, acute illnesses, childbirth, surgical procedures, nutritional deficiencies, and certain pharmacological treatments. Although the hair loss can appear dramatic, it is often reversible, with gradual regrowth once the underlying cause is identified and addressed (50–52).

Anagen Effluvium: A form of abrupt and extensive hair loss that occurs when hair follicles are disrupted during the anagen (growth) phase, typically following exposure to toxic or pharmacological agents. The most common causes include chemotherapy, radiation therapy, certain cytotoxic drugs, and severe toxic exposures (e.g., thallium, arsenic). Hair is shed in large quantities, sometimes in clumps, and may result in partial or complete scalp alopecia. Although the hair loss can be dramatic, it is often reversible if the follicle remains intact, with regrowth typically initiating a few weeks after cessation of the insult (53,54).

Primary scarring alopecia: A rare group of inflammatory scalp disorders that lead to irreversible hair loss due to the destruction of hair follicles, which are replaced by scar tissue. Affecting fewer than 3% to 7% of the global population, PCA can impact both men and women, typically appearing in adulthood (55). Subtypes include Lichen planopilaris (LPP), more common in middle-aged women (56); Frontal fibrosing alopecia (FFA), often affecting postmenopausal women (57); and Central centrifugal cicatricial alopecia (CCCA), predominantly affecting women of African descent (58). Early intervention is crucial to halt progression and preserve remaining hair (59).

Secondary scarring alopecia: Irreversible hair loss resulting from external insults or underlying medical conditions that damage and destroy hair follicles, subsequently replacing them with fibrotic scar tissue. Common etiologies include physical trauma (burns, surgical wounds, radiation), severe infections (inflammatory tinea capitis, bacterial abscesses), dermatologic diseases (cutaneous lupus erythematosus, sarcoidosis), and neoplastic processes affecting the scalp (60,61).

VineOxyl is a hydroxylated grape seed oil enriched in 13-hydroxy-9-octadecenoic acid, a hydroxylated free fatty acid. This active was obtained from grape seed oil using a two-step enzymatic process. First, the grape seed oil was hydrolyzed to release free fatty acids. Then, a specific hydroxylation of linoleic acid into 13-hydroxy-9-octadecenoic acid was carried out. This active ingredient is present in both the shampoo and the serum.

Derived from organic chia seeds (Peru, Brazil, Bolivia) and peas (France), this active ingredient contains peptides, amino acids, oligosaccharides, polyphenols, and minerals, providing antioxidant, soothing, and anti-hair-loss protection. It is produced in France and is 99% of natural origin.

In the anti-hair-loss serum, Procataline G2 was added in complement to VineOxyl.

Hair loss frequently results from an imbalance in the biological mechanisms involved in hair follicle growth and survival. Among these mechanisms, two mediators play a central role: VEGFα and PGE2. VEGFα is a key factor in perifollicular angiogenesis. It promotes vascularization around the hair follicle, enhances nutrient and oxygen supply, and thereby supports the initiation and maintenance of the follicle in the anagen phase. Reduced VEGFα expression is associated with follicle weakening and decreased hair growth. PGE2, meanwhile, is a prostaglandin known for its positive role in stimulating hair growth. It promotes anagen phase, supports dermal papilla cell activity, and counteracts inhibitory prostaglandins involved in certain types of alopecia.

Hair loss is frequently associated with a disruption of the hair cycle, characterized by a shortening of the growth phase. VineOxyl acts on this mechanism by stimulating hair follicle elongation in vitro and ex vivo, while also upregulating key growth-associated genes including FGF7 (Fibroblast Growth Factor 7), PCNA (Proliferating Cell Nuclear Antigen), and HIF-1A (Hypoxia-Inducible Factor-1α).

With age, the hair fiber undergoes a progressive increase in porosity due to cuticle degradation and reduced lipid cohesion. This fragility makes the hair shaft more vulnerable to mechanical, chemical, and environmental stress, leading to increased breakage. Combined with the gradual decline in follicular activity, this weakened structure contributes to visible loss of density and more pronounced hair shedding. VineOxyl acts on this mechanism by reducing hair-fiber porosity after thermal stress exposure, both in leave-on (cream) and rinse-off (shampoo) formulations.

Tested at 1% in vitro, this active ingredient stimulates microcirculation by increasing VEGFα synthesis in dermal papilla cells exposed to pollutant-induced stress, and it also protects hair follicle stem cells from pollutant stress through the regulation of Sox9, a key stem-cell marker. Tested at 1% in vivo, it significantly reduces protein carbonylation after pollution exposure, demonstrating antioxidant activity on the scalp after a single application. Finally, when applied at 1% in a serum for 42 days, it significantly hydrates the scalp, reduces sebum levels, and makes hair loss visibly less noticeable, based on both self-assessment and expert panel evaluation (Ashland supplier documentation).

VineOxyl at 0.002% induced a significant increase in PGE2 secretion, reaching a level 20-fold higher than that of untreated cells.

Treatment with 0.002% VineOxyl (equal to 27 µM of active molecule) increased VEGFα gene expression by 20%, while 100 µM Minoxidil increased it by 30%. Despite this numerical difference, statistical analysis showed no significant difference between the two treatments, indicating comparable efficacy and demonstrating that VineOxyl is as effective as minoxidil, but at a dose three times lower.

Both treatments (VineOxyl and pea extract reference) significantly enhanced hair growth after 10 days, showing a similar efficacy of 16% compared with untreated follicles. However, VineOxyl exhibited a significant effect as early as day 7 (with a 14% increase in hair growth compared with untreated follicles), whereas the reference ingredient showed no effect at day 7, suggesting that VineOxyl promotes hair growth more rapidly.

In an ex vivo scalp model, treatment with VineOxyl induced a 44% increase in hair length between day 2 and day 5 of treatment. Castor oil, meanwhile, induced a 30% increase, which remained non-significant compared with the placebo.

After 5 days of culture, treatment with 0.1% VineOxyl induced:

Treatment with the cream containing 0.05% VineOxyl reduced hair-fiber porosity by 92%, with an effect significantly superior to the placebo. This result demonstrates that leave-on VineOxyl exhibits a reparative effect on hair fibers damaged by thermal stress.

Treatment with the shampoo containing 0.05% VineOxyl reduced hair-fiber porosity by 88%, with an effect significantly superior to the placebo. This result shows that VineOxyl also provides a reparative effect on hair fibers damaged by thermal stress when used in a rinse-off formulation.

The product was applied daily for 3 months directly to the scalp—line by line on dry or damp hair using three pipettes—followed by gentle massage and a 10-minute leave-on period. Dermatologically supervised tolerance assessments at T0 and T28 confirmed excellent tolerability, with no adverse events reported after 28 days.

Clinical evaluation performed by a trained expert through visual analogue scales (VAS) for density, thickness, and volume parameters.

Hair fall evaluated by counting the number of falling hairs from the root under standardized brushing. After 90 days of treatment, the product significantly decreases hair fall by 53%.

The product was applied for a period of 4 months, at a frequency of 2 to 3 uses per week. It was applied to wet hair and gently massaged in circular motions, starting at the nape of the neck and moving up toward the top of the head, with particular attention to areas affected by hair loss. It was then left on for 2 minutes before being thoroughly rinsed. Dermatologically supervised tolerance assessments conducted after 112 days of use confirmed excellent tolerability.

After 28 days of use:

Hair density was assessed after 84 and 112 days using MicroCamera i-Scope USB (Moritex).

The product also showed an improvement in root volume.