Sphingolipid based hair treatment

A sphingolipid-based hair treatment stimulates hair growth, reduces loss, and improves hair quality by enhancing cellular proliferation and inhibiting inflammatory interleukins, addressing the limitations of existing treatments.

WO2026099172A1PCT designated stage Publication Date: 2026-05-15SEDERMA SA +1
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Patent Information

Authority / Receiving Office
WO · WO
Patent Type
Applications
Current Assignee / Owner
SEDERMA SA
Filing Date
2025-11-04
Publication Date
2026-05-15

AI Technical Summary

Technical Problem

Existing hair treatments fail to effectively stimulate hair growth, slow down hair loss, and maintain hair quality while minimizing side effects such as irritation and allergy risks, particularly due to external agents and aging-related hair damage.

Method used

A hair treatment using sphingolipids, specifically ceramides with a sphingoid base and a fatty acid chain, to stimulate hair growth and prevent loss by increasing proliferation of mesenchymal cells in the papillary dermis and inhibiting pro-inflammatory interleukins, while improving scalp health and hair quality.

Benefits of technology

The treatment enhances hair growth, reduces hair loss, improves hair quality by making it softer, shinier, and easier to detangle, while maintaining scalp health by reducing oxidative stress and inflammation.

✦ Generated by Eureka AI based on patent content.

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Abstract

The present invention provides the use of at least one sphingolipid for a hair treatment for inducing hair growth and / or inhibiting hair loss, including eyelashes and eyebrows. Said sphingolipid is preferably a ceramide having a fatty acid with a long hydrocarbon chain of C18-C24, mostly C20-C22, and a phytosphingosine base. Furthermore, and advantageously, the treatment is global, capable to also improve the properties of the scalp and hair themselves.
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Description

[0001] DESCRIPTION

[0002] TITLE: Sphingolipid based hair treatment

[0003] The present invention relates to a hair treatment based on at least one sphingolipid, i.e. a hear treatment for both head hair and body hair, including eyelashes and eyebrows.

[0004] The present invention relates to cosmetic, hygiene and personal care, and dermopharmacy product industries, intended for humans and animals.

[0005] Sphingolipids constitute a particular type of lipids existing for example in the cell membranes of almost all living organisms and collectively refer to various derivatives comprising sphingoid bases as a skeleton (in particular sphingosine, sphinganine or phytosphingosine), fatty acids and polar groups.

[0006] Among these sphingolipids, there are several categories such as sphingomyelins, glycosphingolipids or cerebrosides, gangliosides, globosides or ceramides.

[0007] In the field of cosmetics, sphingolipids are commonly found as active ingredients in skin care products.

[0008] Ceramides are part of the natural components of the stratum corneum, often recommended in moisturizing products and more particularly in anti-aging products to restore the cutaneous hydrolipidic film. This effectively prevents dehydration and protects the skin against external aggressions.

[0009] Ceramides are also widely used in hair products to treat the hair itself. They provide softer, shinier, better hydrated hair with less frizziness. Ceramides with sphinganine as the sphingoid base are the most recommended.

[0010] The use of sphinganine is also known in hair care products. For example, the

[0011] WO2013 / 017361 patent application describes the use of sphinganine to improve the visual appearance of hair by reducing sebum production. In addition, in the WO2015 / 014558 patent application, sphinganine is combined with another active ingredient (creatine, creatine hydrates or disodium phosphocreatine) to stimulate hair growth.

[0012] The WO2022 / 107866 patent application also describes the use of phytosphingosine to stimulate hair growth.

[0013] Hair (of head or body) comprise two parts: the hair follicle (or pilary follicle) and the shaft (or hair fiber), as well as annexes, the most important of which being the sebaceous gland which plays a lubricating role and the arrector muscle which stimulates the secretion of sebum by the sebaceous gland. To simplify the rest of the description, the terms "hair" or "hairs" will be used interchangeably to include any kind of hair: "hairs of the head, including eyelashes and eyebrows and hairs of the body".

[0014] The follicle is the non-visible part. It is divided into three segments, from top (epidermis) to bottom (dermis):

[0015] - The infundibulum is the superficial part of the hair follicle between the surface of the epidermis and the sebaceous gland.

[0016] - The isthmus is located in the dermis, between the sebaceous gland and the insertion site of the arrector muscle. This insertion site, also called the bulge, is a stem cell niche.

[0017] - The bulb is located in the dermis, below the bulge. At the base of the bulb is the papillary dermis composed of mesenchymal cells called HFDPCs (Human Follicle Dermal Papilla Cells) that interact with the other cells of the bulb to induce hair growth. The papillary dermis also contains blood vessels to provide nutrients and oxygen necessary for the growth of the hair shaft or fiber. Above and around the dermal papilla is a so-called germinative zone containing stem cells (keratinocytes, melanocytes and matrix cells). The keratinocytes in the germinative zone are pigmented by neighboring melanocytes. These keratinocytes enter the phase of differentiation and apical migration to give rise to the keratogenic zone where keratin is produced. The matrix cells proliferate and differentiate, giving rise to the shaft.

[0018] The hair shaft or fiber is the visible part that is outside the hair follicle. It is composed of three layers, from the outside to the inside:

[0019] - The cuticle is composed of cells arranged in scales to protect the hair from external aggressions.

[0020] - The cortex is composed of cortical cells having a fibrous character, fusiform in shape, sealed and embedded in each other. The cortex gives color, solidity and resistance to the hair.

[0021] - The medulla is composed of medullary cells which are degenerated cells and replaced by large vacuoles filled with air and a few grains of melanin.

[0022] Hair growth and renewal are mainly determined by the activity of hair follicles and their matrix environment. Their activity is cyclical and essentially comprises three phases, namely the anagen phase, the catagen phase and the telogen phase, which are repeated until the death of the hair. Thus, hair does not grow continuously, but in successive cycles. This cycle is repeated between twenty-five- and thirty-times during life, thanks to the regenerative capacity of the follicle stem cells that reside in the bulb region. The hair cycle begins with the phase called anagen corresponding to strong growth of the hair inside its hair follicle. It lasts on average from 2 to 5 years. 85% to 90% of hair is usually in the anagen phase. During this phase, the hair bulb regenerates and then produces the hair fiber. The hair thus grows approximately one cm per month. This is a highly proliferative phase that results from the proximity between the dermal papilla, in contact with the blood vessels, and the bulge where the hair stem cells are located. From there, the production of the fiber will be generated thanks to the intense production of keratin and keratinocytes which then form the external cuticles of the hair and the cortex.

[0023] At the end of this anagen phase, the follicle enters a regression phase called the catagen phase and syntheses are stopped. The fiber no longer grows due to a lack of supply to the dermal papilla by the blood vessels. This phase only lasts a few weeks and concerns approximately 2% to 3% of the hair at any given time. The follicle gradually retracts and involutes. The keratinocytes and melanocytes gradually disappear, and the bulb collapses on itself while retaining the dermal papilla.

[0024] Then, the dermal papilla begins to rise towards the bulge. This is the phase called telogen which precedes a new anagen phase. 8% to 10% of hair is in the telogen phase at any given time. It remains there for about 6 to 7 months in young people but longer as they age.

[0025] This hair cycle is the same for head hair and body hair with different phase and therefore cycle durations, in particular the duration of the anagen phase is shorter for body hair.

[0026] Hair is generally damaged and weakened by the action of external atmospheric agents such as light and bad weather, as well as by mechanical or chemical treatments such as brushing, combing, dyeing, bleaching, perming and / or straightening, or even repeated washing.

[0027] In addition, with ageing, hair becomes thinner and its cycles shorter.

[0028] Hair is thus damaged and can become dry, rough, brittle, dull or lead to hair loss reducing hair density.

[0029] To overcome these drawbacks, it is common to use products intended for treating the hair or scalp, such as plant extracts, pure synthetic molecules, vitamins and keratin hydrolysates with various sulfur compounds.

[0030] There is therefore always a need for effective products that reduce side effects such as the risks of irritation and allergy, to preserve and / or improve the general condition of the hairs and / or body hair,

[0031] The present invention therefore aims to propose a hair treatment, and more particularly a treatment to induce hair growth and slow down hair loss, while preserving the quality and beauty of the scalp. To this end, according to a first object, the present invention proposes the use of at least one sphingolipid for a non-therapeutic cosmetic hair treatment to induce hair growth or body hair and / or slow down hair loss.

[0032] The application of this treatment is particularly interesting for head hair, as well as for eyelashes and eyebrows.

[0033] Preferably, the sphingolipid comprises a fatty acid chain portion that comprises from 16 to 24 carbon atoms and / or comprises phytosphingosine as sphingoid base.

[0034] The ceramides comprise a sphingoid base and a fatty acid linked by an amide bond.

[0035] Preferably according to the invention, the sphingolipid is a ceramide, which may be natural or synthetic, and be a pseudo-ceramide having a structure similar to that of ceramides.

[0036] More specifically, the sphingolipid used in the treatment according to the invention is a ceramide of the following general formula (1): in which:

[0037] R1 is -CH2-CH2-, -CH=CH- or -C(H)OH-CH2-;

[0038] R2 is an alkyl, alkenyl or alkynyl chain, having from 10 to 20 carbon atoms, which may be linear or branched;

[0039] -CO-R3 is a fatty acid chain having from 12 to 28 carbon atoms (including the carbon of CO), R3 being an alkyl, alkenyl or alkynyl hydrocarbon chain which may be linear or branched, and optionally substituted by a hydroxyl group; and

[0040] R4 is H or an alkyl, alkenyl or alkynyl chain, having from 1 to 10 carbon atoms, or an acylated or dehydrogenated derivative of this ceramide

[0041] The sphingoid base of the ceramide can be chosen from:

[0042] - a sphingosine type base corresponding to R1=-CH=CH-,

[0043] - a phytosphingosine type base corresponding to R1=-C(H)OH-CH2-; or

[0044] - a sphinganine type base (also called dihydrosphingosine) corresponding to R1=-CH2- CH2-. Preferably, the sphingoid base is a phytosphingosine type base corresponding to R1=-C(H)OH-CH2-.

[0045] Preferably, in the sphingoid base, R4 is H or an alkyl chain of 1 to 6 carbon atoms, preferably a linear chain, more preferably R4 is H or a linear alkyl chain of 1 to 3 carbon atoms, preferably 1 carbon atom, and more preferably R4 is H.

[0046] Preferably, R2 is an alkyl, alkenyl or alkynyl chain, having from 12 to 16 carbon atoms.

[0047] Preferably R2 is a linear chain.

[0048] Preferably, the sphingoid base is selected from sphingosine also called sphingenine (corresponding to R1=-CH=CH-, R4=H and R2=C13H25), sphinganine (R1-CH2-CH2-, R4=H and R2=C13H25) and phytosphingosine (corresponding to R1=-C(H)OH-CH2-, R4=H and R2=C13H25). More preferably, the sphingoid base is phytophingosine. The present invention also covers acylated ceramide derivatives, namely having an acylated sphingoid base, in particular acetylated, mono, di or tri, where appropriate, or dehydrogenated ceramide derivatives, namely having a dehydrogenated sphingoid base, such as dehydrosphingosine, dehydrosphinganine or dehydrophytosphingosine.

[0049] In the ceramide, the fatty acid part comprises a hydrocarbon chain (corresponding to R3 in formula 1), which may be saturated, unsaturated, for example by a double bond or a triple bond, and / or hydroxylated. Preferably according to the invention, the fatty chain R3 is saturated.

[0050] Preferably according to the invention, the carbon fatty acid chain -CO-R3 comprises an even number of carbons.

[0051] Preferably according to the invention, the hydrocarbon chain R3 is linear. More preferably, the carbon fatty acid chain -CO-R3 is a long chain, that is to say that it contains at least 16 carbon atoms, more preferably at least 18 carbon atoms and more preferably at least 20 carbon atoms.

[0052] More preferably, the fatty acid chain -CO-R3 comprises from 14 to 26 carbon atoms, more preferably from 16 to 24 carbon atoms, more preferably from 20 to 24 carbon atoms, more preferably from 20 to 22 carbon atoms.

[0053] According to a particularly interesting embodiment for implementing the invention, the treatment according to the invention uses a mixture of sphingolipids which is composed of ceramides which have a fatty acid part -CO-R3 having a chain of 16 to 24 carbon atoms, of which at least 70% have a chain of 20 to 22 carbon atoms, preferably at least 80%, and more preferably at least 90%. Preferably, the treatment according to the invention uses a mixture of sphingolipids which is composed of ceramides which have a fatty acid part -CO-R3 having 16, 18, 20, 22 and 24 carbon atoms, of which at least 70% have a chain of 20 and 22 carbon atoms, preferably at least 80%, and more preferably at least 90%.

[0054] More particularly, the treatment according to the invention uses the mixture of ceramides having the following distribution of fatty acid chains:

[0055] - C16 fatty acid at a content in % by weight of 0 to 4%;

[0056] - C18 fatty acid at a content in % by weight of 7 to 12%;

[0057] - C20 fatty acid at a content in % by weight of 36 to 45%;

[0058] - C22 fatty acid at a content in % by weight of 37 to 48%; and

[0059] - C24 fatty acid at a content in % by weight of 0 to 4%.

[0060] Furthermore, preferably, the ceramides of the mixture are NP-type ceramides (also called ceramides 3) comprising the same phytosphingosine base.

[0061] Thus, according to a second aspect, the present invention proposes a hair composition suitable in particular for the treatment according to the invention comprising:

[0062] - a mixture of ceramides as defined above; and

[0063] - a physiologically acceptable medium comprising a surfactant. in particular, this composition comprises a mixture of ceramides whose hydrocarbon chain of the fatty acid part comprises from 16 to 24 carbons and more particularly a hydrocarbon chain of the fatty acid part which comprises at least 70% of a chain with 20 and 22 carbons and a phytosphingosine as a sphingoid base.

[0064] This composition may be, for example, a shampoo or a conditioning agent to be rinsed or not, such as a conditioner.

[0065] Preferred aspects of this composition as well as other compositions according to the invention are detailed below in the description. Similarly, test results are given below in the detailed description showing the effect according to the invention on hair growth and hair loss, in particular as summarized below.

[0066] At the cellular level, it has been shown that the use of a sphingolipid according to the invention increases the proliferation of mesenchymal cells of the papillary dermis of the bulb (HFDPCs). These cells are necessary for the development of hair follicles. They are also capable of sending signals to hair stem cells to activate their growth. Thus, increasing their proliferation stimulates hair growth and morphogenesis. At the gene level, an increase in the expression of two genes responsible for hair shaft morphogenesis has been shown:

[0067] - the FGF7 gene, promoting the proliferation of HFDPCs and regulating the proliferation and differentiation of hair follicle stem cells; and

[0068] - the Noggin gene stimulating the induction of the hair follicle by promoting the transition from the telogen phase to the anagen phase.

[0069] Furthermore, it is known that hair protects the scalp, but it is less known that the quality of the scalp is just as important to provide a good incubating environment for the production of beautiful and healthy hair.

[0070] To this end, the scalp must be protected from the various stresses that can weaken it. These stresses directly or indirectly impact the hair follicles and cause hair growth and loss problems. Hair growth is stopped by an induction of the catagen phase and / or by a shortening of the anagen phase. These events are also correlated with a decrease in the proliferation of HFDPCs.

[0071] For example, oxidative stress generated by exposure to UV radiation, exposure to air pollution or oxidizing compounds, such as reactive oxygen species, has a harmful effect on the human body in general, but also on the hair and scalp.

[0072] Stress due to irritation, whether due to an irritating external factor or to physical or chemical treatment, also weakens the scalp.

[0073] Inflammatory stress, such as atopic dermatitis, induces the catagen phase in the follicle and weakens the scalp.

[0074] These stresses responsible for weakening the scalp are often associated with discomfort such as itching, dryness and / or hyper-seborrhea of the scalp linked to its irritation, and also cause a decrease in the vigour and a dull appearance of the hair, or even premature hair loss.

[0075] At the cellular level, there are various active substances involved in cellular interactions and influencing surrounding cells. Pro-inflammatory cytokines are known to cause various inflammatory symptoms including, ultimately, hair loss. Among these inflammatory cytokines, there are many interleukins, noted IL.

[0076] The tests given below in the description show an inhibition of pro-inflammatory interleukins which are increased in the event of stress, and which are important for improving the quality of the scalp, the anchoring of hair follicles and ultimately slowing hair loss. In particular, it has been shown according to the invention an action on: - IL-1 a which has the main activity of inhibiting the growth of hair follicles, and as a secondary activity which occurs later of also inhibiting the growth of the hair shaft, this interleukin also causing itching;

[0077] - 1 L-1 p known to induce the catagen phase in cells which is the regression phase of the hair follicle;

[0078] - IL-4 which induces apoptosis in follicular keratinocytes, but not in the cells of the dermal papilla; this IL-4-mediated apoptosis participates in the entry into the catagen phase of the hair follicle by acting selectively on follicular keratinocytes in culture;

[0079] - IL-6 which causes a strong inflammatory response that progressively exhausts peripheral cells, and when it is localized in the scalp, the exhaustion of the hair follicles ultimately leads to hair loss due to miniaturization of the follicle;

[0080] - IL-8 which is a mediator found at high levels in the scales of people with dandruff; the formation of IL-8 also induces hyperproliferation of cells with the consequence of an alteration of the barrier function and sensitization of the scalp to aggressions; and

[0081] - 1 L-13 which is a mediator strongly present in people with atopic dermatitis, more particularly in the lesions caused by atopic dermatitis; atopic dermatitis is characterized by severe itching caused by tissue inflammation; when the person scratches, it causes lesions in the scalp, making it more sensitive to attacks and leading to poorer anchoring of the hair follicle or even leading to its loss.

[0082] In addition, it has been shown to have a favorable effect on two genes involved in alopecia. Inhibiting these two genes, which are increased in cases of stress, is important for improving the formation of hair follicles and slowing hair loss:

[0083] - the TRPV3 gene, for Transient receptor potential cation channel, subfamily V, member 3, codes for the protein of the same name; this gene is expressed in follicular keratinocytes; an increase in the TRPV3 protein leads to an inhibition of hair shaft elongation, a suppression of proliferation, an induction of apoptosis and a premature regression of the hair follicle; and

[0084] - the TARC gene, for Thymus and activation-regulated chemokine, which is responsible for the production of the CCL17 protein, C-C motif chemokine 17", strongly present in people with atopic dermatitis or alopecia aerata.

[0085] The hair follicle is found in the skin, and consequently interacts with the cells and the cellular matrix of the scalp. As a result, the quality of the skin of the scalp impacts the quality of the growth and morphology of the hair. As for the hair, its structure is also impacted by the quality of the scalp. It has been observed that the structure of the hair of patients with psoriasis or atopic or seborrheic dermatitis is different from that of individuals without any of these pathologies. Furthermore, it has been observed that a treatment reducing the oxidative stress of the scalp helps improve the appearance of the hair.

[0086] In addition, there are other proteins, such as involucrin, loricrin and filaggrin, that are responsible for the good quality of the barrier function and improve the hydration of the stratum corneum. Thus, the increase in these proteins is also important in complement to a better quality of the scalp, which allows the hair follicle and therefore the hair to be better anchored and prevents hair loss. The tests given below in the description show an increase in the synthesis of these proteins.

[0087] Finally, an optimal skin barrier function is ensured by scalp desquamation, which eliminates superficial cells in a non-visible and imperceptible manner. However, loss of barrier integrity is often observed in dandruff conditions. In these conditions, the division of cells in the basal layer of the epidermis becomes too rapid, the cells that rise to the surface of the skin do not have time to finish maturing and transform into small corneocytes. Instead, larger and therefore more visible cellular structures with a remaining nucleus (dandruff) are formed. This abnormal acceleration of desquamation facilitates the penetration of molecules and external agents that can irritate the scalp. This results in a disruption of the protective and regulatory functions of the stratum corneum.

[0088] If the barrier function of the scalp is impaired, then desquamation is not occurring normally, and inflammation of the scalp occurs, resulting in an increase in temperature at the scalp level.

[0089] It has been shown that by applying the treatment according to the invention, a sensory soothing is observed that can be measured by a decrease in the temperature of the scalp, and visually by better hydration and a reduction in dandruff.

[0090] The treatment according to the invention is therefore suitable for promoting the anchoring of hair follicles in the scalp.

[0091] The treatment according to the invention is also effective on scalp microbiome. Results of tests are given below showing that the sphingolipid of the invention can act on several microorganisms present in scalp microbiome, C. acnes, S. epidermidis and S. aureus, helping to restore the microbiome balance, in particular the ratio C. acnes / S. epidermidis, and therefore preventing scalp sensitive symptoms directly linked to hair loss and / or reducing hair growth. The treatment of the invention can also down regulate sebum production. Advantageously, the tests show that the treatment according to the invention is a global treatment in that it is not only suitable for slowing down hair loss and improving its growth as explained above, but it is also suitable for improving the moisturizing properties of the scalp and the hair itself, and the quality of the hair (shine, softness, protection following thermal exposure, hair surface repair / smoothness or strengthening of hair fiber after UV-induced damage).

[0092] In vitro and in vivo test results are given below in the description to demonstrate these specific cosmetic activities, beneficial for the hair and scalp. The detailed description also presents an ex vivo study on the improvement of the condition of the scalp on reconstructed epidermis.

[0093] At the hair level, the tests below present the use of a sphingolipid according to the invention allowing to obtain hair that is more hydrated, shinier, softer and easier to detangle. Indeed, by smoothing the hair scales, this makes it possible to retain hydration, to better reflect light, to prevent the scales from clinging to each other and thus tangling the hair.

[0094] Thus, the treatment according to the invention is suitable for increasing the hydration, shine, and / or softness of the hair, as well as facilitating its detangling.

[0095] According to the invention, the use of at least one sphingolipid as defined above is proposed for the preparation of a hair composition, preferably a hair composition, recommended for the topical non-therapeutic cosmetic treatment intended to stimulate the growth of hair and body hair and / or to prevent their loss, said composition comprising at least one sphingolipid and a physiologically acceptable medium.

[0096] By "topical treatment" or "topical use" is meant according to the invention an application which is intended to act at the place where it is applied.

[0097] By "physiologically acceptable medium" is meant according to the present invention, without being limiting, an aqueous or hydroalcoholic solution, a water-in-oil emulsion, an oil-in-water emulsion, a microemulsion, an aqueous gel, an anhydrous gel, a serum, an oil, a dispersion of vesicles or a powder.

[0098] "Physiologically acceptable" means that the composition is suitable for topical use in contact with mucous membranes, nails, scalp, hair, body hair, including eyelashes and eyebrows, and mammalian and more particularly human skin, without risk of toxicity, incompatibility, instability, allergic response, and others.

[0099] This "physiologically acceptable medium" forms what is conventionally called the excipient of the composition. Depending on the physiologically acceptable medium and the concentration of sphingolipid(s), this composition may constitute a concentrated active ingredient intended to enter into a final composition for a consumer, or may directly constitute said final composition, less concentrated.

[0100] In a composition according to the invention, the sphingolipid(s) may be present at a more or less high concentration depending on its destination, ranging from 10'7% to 20% relative to the total weight of the composition, preferably ranging from 10'6% to 10%, more preferably from 10-5% to 5%, by weight relative to the total weight of the composition.

[0101] For example, in a composition forming an ingredient according to the invention, at least one sphingolipid according to the invention will be present at a high concentration generally ranging from 100 ppm to 20,000 ppm, preferably ranging from 100 ppm to 5,000 ppm, more preferably from 100 ppm to 1,000 ppm. This ingredient will then be formulated generally between 0.01% and 10%, preferably between 0.1% and 5% in the final topical preparation.

[0102] When several sphingolipids according to the invention are present in a composition according to the invention, they may be present in variable relative proportions, in equivalent amounts, or on the contrary in different proportions.

[0103] All the percentages and ratios used in the present application are expressed by weight relative to the total weight of the whole considered, for example of the composition according to the invention, and all measurements are made at 25°C, unless otherwise specified.

[0104] According to a particular aspect of the invention, the sphingolipid(s) according to the invention may be solubilized in a lipophilic or hydrophilic matrix with, where appropriate, a solubilizer, depending on the intended application. The sphingolipid(s) in the treatment according to the invention may be combined with other active ingredients at effective concentrations that can act synergistically or as a reinforcement to achieve the desired effects described for the invention, such as the following agents: filtering radiation, in particular UVA, UVB, I R, from blue light, myorelaxant, restructuring, acting on microcirculation, acting on the skin microbiome, acting on inflammation, on free radicals, vitamins, anti-wrinkle, calming, moisturizing, antioxidant, promoting growth, anti-hair loss, anti-dandruff, restoring skin flora, acting on cuticles, on the softness and silky appearance of hair and body hair, etc. These active ingredients can be obtained by synthesis or from natural materials, such as plant extracts or in vitro plant culture products or fermentation products.

[0105] More particularly, in the cosmetic treatment according to the invention to improve or beautify the general condition of the hair and body hair, the sphingolipid according to the invention can be combined, without this list being exhaustive, with one or more of the following active ingredients:

[0106] - an anti-dandruff active ingredient acting as an antifungal: such as Zinc Pyrithione, Ketoconazole, Climbazole, Piroctone Olamine, Selenium Disulfide or Pycnidione; and / or

[0107] - an active ingredient that slows down or inhibits the development of yeasts responsible for dandruff (of the Malassezia genus) and / or acts favourably on the skin barrier, such as the peptide Pal-KTTKS (SEQ ID NO: 1) (Matrixyl®) or Pal-KTSKS (SEQ ID NO: 2) (BB-Biont™), or APISCALP™, active ingredients sold by SEDERMA; and / or

[0108] - a moisturizing active ingredient such as DuraQuench IQ™ (CRODA) or UNSAPONIFIABLE KARITE (Sederma); and / or

[0109] - an active ingredient that rebalances the skin microflora such as the active ingredient HAIRSPA™ (SEDERMA); and / or

[0110] - a calming active ingredient such as PACIFEEL™ (SEDERMA); and / or

[0111] - an active ingredient to prevent hair loss and stimulate hair growth such as CAPIGENE™, CAPILECTINE™, PROCAPIL™ (SEDERMA), or the peptide Pal-GQPR (SEQ ID NO: 3); and / or

[0112] - an active ingredient to strengthen the structure of damaged hair such as CERAMIDE A2™, CERAMIDE HO3™, HELIOGENOL™ (SEDERMA); and / or

[0113] - an active ingredient to smooth hair such as FRUIT BIO™ (SEDERMA); and / or

[0114] - an active ingredient to protect hair and body hair, including eyelashes and eyebrows, from UV and IR radiation such as VENUCEANE™ (SEDERMA); and / or

[0115] - an agent to repigment hair and body hair, including eyelashes and eyebrows, such as SILVERFREE ™ (SEDERMA).

[0116] Detailed examples are given in the formulation section below.

[0117] The Personal Care Products Council ("International cosmetic ingredient dictionary & handbook" published by "the Cosmetic, Toiletry, and Fragrance Association, Inc.", Washington, D.C.) describes a wide variety, without limitation, of cosmetic and pharmaceutical ingredients commonly used in the personal care industry, which are suitable for use as additional ingredients in the compositions according to the present invention, as long as they are physically and chemically compatible with the other ingredients of the composition and especially with the active ingredients of the present invention. Furthermore, the nature of these additional ingredients must not alter the benefits of the active ingredients of the invention. These additional ingredients may be synthetic or natural, such as plant extracts or come from a biofermentation process.

[0118] Other skin care active ingredients, including scalp care active ingredients, which are particularly useful in combination with the composition according to the invention can be found in the commercial literature of Sederma, Crodarom and Alban Muller International, and on the website www.croda.com. Other examples of commercial active ingredients include: betaine, glycerol, Actimoist Bio 2™ (Active organics), AquaCacteen™ (Mibelle AG Cosmetics), Aquaphyline™ (Silab), AquaregulK™ (Solabia), Carciline™ (Greentech), Codiavelane™ (Biotech Marine), Dermaflux™ (Arch Chemicals, Inc), Hydra’Flow™ (Sochibo), Hydromoist L™ (Symrise), RenovHyal™ (Soliance), Seamoss™ (Biotech Marine), Argireline™ (trade name for Lipotec’s acetyl hexapeptide- 3), spilanthol or an extract of Acmella oleracea known as Gatuline Expression™, an extract of Boswellia serrata known as Boswellin™, Deepaline PVB™ (Seppic), Syn-AKE™ (Pentapharm), Ameliox™, Bioxilift™ (Silab), PhytoCellTec™Argan (Mibelle), Papilactyl D™ (Silab), Preventhelia™ (Lipotec), or one or more of the following active ingredients sold by Sederma: Subliskin™, Venuceane™, Moist 24™, Vegesome Moist 24™, Essenskin™, Juvinity™, Revidrat™, Resistem™, Chronodyn™, Kombuchka™, Chromocare™, Calmosensine™, Glycokin factor S™, Biobustyl™, Idealift™, Ceramide 2™, Ceramide A2™, Ceramide H03™, Legance™, Intenslim™, Prodizia™, Beautifeye™, PacifeelTM, Zingerslim™, Meiritage™, Sebuless™, Apiscalp™, Rubistem™, Citystem™, Neonyca™, NG Shea Butter Unsaponifiables™, Majestem™, Hydronesis™, Poretect™, Amberstem™, Synchrolife™, Feminage™, Sylverfree™, Ameyezing™, Revitalide™, Mel[o]stem™, Luceane™ or mixtures thereof. Among the plant extracts (in the form of conventional extracts or prepared by an in vitro method) which may be used as additional active agents, mention may also be made in particular of ivy extracts, for example climbing ivy (Hedera helix), Bupleurum chinensis, Bupleurum falcatum, arnica (Arnica montana L.), rosemary (Rosmarinus officinalis N.), marigold (Calendula officinalis), sage (Salvia officinalis L.), ginseng (Panax ginseng), ginko biloba, St. John's wort (Hyperycum perforatum), butcher's broom (Ruscus aculeatus L.), meadowsweet (Filipendula ulmaria L.), orthosiphon (Orthosiphon stamincus Benth.), artichoke (Cynara scolymus), algae (Fucus vesiculosus), birch (Betula alba), green tea, kola nut (Cola nipida), horse chestnut, bamboo, Centella asiatica, heather, fucus, willow, pilosella, escin extracts, cangzhu extracts, Crysanthellum indicum extracts, plants of the Armeniacea genus, Atractylodis platicodon, Sinnomenum, pharbitidis, Flemingia, from Coleus like C. forskohlii, C. blumei, C. esquirolii, C. scutellaroides, C. xanthantus and C. barbatus, like extract from roots of Coleus barbatus, extracts from Ballote, Guioa, Davallia, Terminalia, Barringtonia, Trema, Antirobia, Cecropia, Argania, Dioscoreae like Dioscorea opposita or Mexican, extracts of Ammi visnaga, of Siegesbeckia, in particular Siegesbeckia orientalis, plant extracts of the Ericaceae family, in particular extracts of blueberries (Vaccinium angustifollium) of Arctostaphylos uva ursi, Aloe vera, of plants containing sterols (in particular phytosterols), of Manjistha (extract of plants of the genus Rubia, in particular Rubia cordifolia), of Guggal (extract of plants of the genus Commiphora, in particular Commiphora mukul), an extract of kola, chamomile, red clover, of Piper methysticum (Kava Kava of Sederma), of Bacopa monieri (Bacocalmine™, Sederma) and of sea whip, of Glycyrrhiza glabra, of mulberry, of melaleuca (tea tree), of Larrea divaricata, of Rabdosia rubescens, of Euglena gracilis, of Fibraurea recisa hirudinea, Chaparral sorghum, sunflower flower, Enantia chlorantha, Mitracarp of the genus Spermacocea, Buchu barosma, Lawsonia inermis L., Adiantium capillus-veneris L., Chelidonium majus, Luffa cylindrica, “Japanese Mandarin” (Citrus reticulata bianco var. unshiu), Camelia sinensis, Imperata cylindrical, Glaucium flavum, Cupressus sempervirens, Polygonatum multiflorum, Lovely hemsleya, Sambucus nigra, Phaseolus lunatus, Centaurium, Macrocystis pyrifera, Turnera diffusa, Anemarrhena asphodeloides, Portulaca pilosa, Humulus lupulus, Arabica coffee, Ilex paraguariensis, Globularia cordifolia, Oxydendron arboreum, Albizzia julibrissin, Zingiber zerumbet smith, Astragalus membranaceus, Atractylodes macrocephalae, Plantago lanceolata, Leontopodium alpinum (or eldelweiss), Mirabilis jalapa, ofApium graveolens, of Marrubium vulgare, Buddleja davidii Franch., Syringa vulgaris, Engelhardia chrysolepsis, Monarda didyma, or orchids.

[0119] The compositions according to the present invention may comprise peptides, including, but not limited to, di-, tri-, tetra-, penta- and hexapeptides and their repeats and derivatives. According to a particular embodiment, the concentration of the additional peptide in the composition varies between 10-7% and 20%, preferably between 10-6% and 10%, preferentially between 10-5% and 5%, by weight.

[0120] Non-limiting examples of dipeptides that can be used in the context of the present invention include Carnosine (P-AH), YR, VW, NF, DF, KT, KC, CK, KP, KK, TT, PA, PM or PP.

[0121] Non-limiting examples of tripeptides include RKR, HGG, GHK, GKH, GGH, GHG, KFK, KAvaK, K AK, KAbuK, KAcaK, KPK, KMOK, KMO2K, PPL, PPR, SPR, QPA, LPA or SPA. Non-limiting examples of tripeptides include:

[0122] - a proline grafted to lysine such as K(P)HG or K(P)GH; or

[0123] - a proglutamic acid grafted to a lysine such as K(Pyr)HG or K(Pyr)GH; or

[0124] - an acetylated lysine such as K(Ac)HG or K(Ac)GH. Non-limiting examples of tetrapeptides are KTFK (SEQ ID NO: 4), RSRK (SEQ ID NO: 5), KTAK (SEQ ID NO: 6), KAYK (SEQ ID NO: 7), KFYK (SEQ ID NO: 8), TKPR (SEQ ID NO: 9), AVPG (SEQ ID NO: 10), VPGA (SEQ ID NO: 11), LKLE (SEQ ID NO: 12), ELED (SEQ ID NO: 13) or LLAN (SEQ ID NO: 14).

[0125] A non-limiting example of a pentapeptide is KTTKS (SEQ ID NO: 15) and KTSKS (SEQ ID NO: 16) and examples of hexapeptides are GKTTKS (SEQ ID NO: 17) and VGVAPG (SEQ ID NO: 18).

[0126] Other peptides that can be used in the context of the present invention may be chosen from, without this list being limiting: lipophilic derivatives of peptides, preferably oleoyl, palmitoyl and myristoyl derivatives, and complexes with the metal ions mentioned above (for example: copper complex of the tripeptide HGG).

[0127] Preferred dipeptides include for example N-Palmitoyl-p-Ala-His, N-Acetyl-Tyr-Arg- hexadecylester (Calmosensine™, Idealift™, Sederma), Pal-KT, Pal-RT, Pal-PP and Pal-PA (Sederma).

[0128] Preferred tripeptides include, but are not limited to, the copper derivative of HGG (Lamin™, Sigma), Pal GHK and Pal GKH (Sederma), lipospondin (N-Elaidoyl-KFK) and its conservatively substituted analogues, N Acetyl RKR NH2 (Peptide CK+), Pal KavaK, Pal KpAlaK, Pal KAbuK, Pal KAcaK, Pal KMO2K (Matrixyl®synthe’6®, Sederma), Pal KVK (Syn- CollTM, DSM), N Biot GHK (Sederma) and their derivatives. Mention may also be made here of the anti-aging tripeptides of general formula X-Pro*-Pro*-Xaa-Y described in application WO2015 / 181688 with Xaa chosen from Leu, Arg, Lys, Ala, Ser, and Asp, at the N-terminal end, X chosen from H, -CO-R1 and -SO2-R1 and at the C-terminal end, Y chosen from OH, OR1 , NH2, NHR1 or NR1 R2, R1 and R2 being, independently of one another, chosen from an alkyl, aryl, aralkyl, alkylaryl, alkoxy and aryloxy group, which may be linear, branched, cyclic, polycyclic, unsaturated, hydroxylated, carbonylated, phosphorylated and / or sulfur-containing, said group possibly having in its skeleton a heteroatom in particular O, S and / or N, and Pro* corresponding to Proline, an analogue or a derivative thereof; including for example Myr-PPL-OH and Myr-PPR-OH. Mention may also be made here of the propigmenting and / or pro-collagen dipeptides and tripeptides of general formula X-(Xaa1)n- Pro*-Xaa2-Y described in application WQ2014 / 080376, with n=0, 1 or 2, Xaa1 a hydrophobic amino acid chosen from Ala, Vai, Met, Leu, Iso, Phe, Pro, and analogues or derivatives thereof; or a polar amino acid chosen from Ser, Thr, Tyr, Asp, Glu and derivatives and analogues thereof; and when n=2 the two Xaa1 amino acids may be identical or different; Xaa2 a hydrophobic amino acid chosen from Ala, Vai, Met, Leu, Iso, Phe, and analogues or derivatives thereof; a basic amino acid chosen from Arg, Lys, His, and derivatives and analogues thereof; at the N-terminal end of the peptide, X is chosen from H, -CO-R1 and -SO2-R1 ; at the C-terminal end of the peptide, Y is chosen from OH, OR1, NH2, NHR1 or NR1R2, R1 and R2 being, independently of one another, chosen from an alkyl, aryl, aralkyl, alkylaryl, alkoxy, saccharide and aryloxy group, which may be linear, branched, cyclic, polycyclic, unsaturated, hydroxylated, carbonylated, phosphorylated and / or sulfur-containing, said group being able to have in its skeleton a heteroatom in particular O, S and / or N; Pro* corresponding to Proline, an analogue or a derivative thereof; comprising for example the peptides Pal-SPR-OH, Pal-PPR-OH, Pal-QPA-OH, Pal-LPA-OH, Myr-SPA- OH, Pal-PM-OH, Pal-PA-OH and Pal-PP-OH. Tetrapeptide derivatives that may be used in the present invention include, but are not limited to, Ela-KTAK (SEQ ID NO: 19), Ela-KAYK (SEQ ID NO: 20), Ela-KFYK (SEQ ID NO: 21) or Pal-KTFK (SEQ ID NO: 22).

[0129] Useful pentapeptide derivatives include, but are not limited to, Pal-KTTKS (SEQ ID NO: 1) (MATRIXYL™, Sederma), Pal-KTSKS (SEQ ID NO: 2), Pal-YGGFXaa (SEQ ID NO: 23) with Xaa being Leu or Pro, or a mixture thereof.

[0130] Useful hexapeptide derivatives include, but are not limited to, Pal-HLDHXaa (SEQ ID NO: 24) with Xaa being Trp, Phe, Tyr, Tic, 7-hydroxy-Tic or Tpi, Pal-GKTTKS (SEQ ID NO: 25), Pal-VGVAPG (SEQ ID NO: 26) (DERMAXYLTM, marketed by Sederma).

[0131] Preferred commercially available compositions offered by Sederma include:

[0132] - tripeptides or derivatives include: Biopeptide-CL™, Maxi-Lip™, or Procapil™ comprising GHK;

[0133] - a tetrapeptide or derivative includes: Crystalide™, which contains Pal-KTFK (SEQ ID NO: 22) carried (solvated in microemulsion)

[0134] - pentapeptides or derivative such as Matrixyl™ source of Pal-KTTKS (SEQ ID NO: 1).

[0135] We can also mention:

[0136] - the mixture Pal-GHK and Pal-GQPR (SEQ ID NO: 3) (Matrixyl™ 3000), and

[0137] - the mixture Pal-GHK and Pal-VGVAPG (SEQ ID NO: 26) (Biobustyl™).

[0138] The following commercial peptides may also be mentioned as additional active ingredients:

[0139] - Vialox™ (INCI name = Pentapeptide-3 (synthetic peptide comprising alanine, arginine, isoleucine, glycine and proline)), Syn-ake™ (P-Ala-Pro-Dab-NH-Bzl) or Syn-Coll™ (Pal-Lys- Val-Lys-OH) sold by Pentapharm,

[0140] - Argireline™ (trade name of Lipotec acetyl hexapeptide-3), Leuphasyl™ (Tyr-D-Ala-Gly- Phe-Leu (SEQ ID NO: 27)), Aldenine™ (Gly-His-Lys), TrylagenTM (INCI name = Pseudoalteromonas Ferment Extract, Hydrolyzed Wheat Protein, Hydrolyzed Soy Protein, Tripeptide-10 Citrulline (product of the reaction of citrulline and Tripeptide-10 (synthetic peptide consisting of aspartic acid, isoleucine and lysine)), Tripeptide-1), Eyeseryl™ (Ac-p- Ala-His-Ser-His (SEQ ID NO: 28)), Serilesine™ (Ser-lle-Lys-Val-Ala-Val (SEQ ID NO: 29)) or Decorinyl™ (INCI name: Tripeptide-10 Citrulline = product of the reaction of Citrulline and Tripeptide-10 (synthetic peptide consisting of aspartic acid, isoleucine and lysine) sold by Lipotec, - Collaxyl™ (Gly-Pro-GIn-Gly-Pro-GIn (SEQ ID NO: 30)) or Quintescine™ (Cys-Gly) sold by the company Vincience,

[0141] - Cytokinol™LS (casein hydrolysate) sold by Laboratoires Serobiologiques / Cognis,

[0142] - Kollaren™ (Gly-His-Lys), IP2000™ (Pal-Val-Tyr-Val) or Meliprene™ (INCI name = Monofluoroheptapeptide-1 : product of the reaction of acetic acid and a synthetic peptide containing arginine, glycine, glutamic acid, histidine, norleucine, p-fluorophenylalanine and tryptophan) sold by the European Institute of Cell Biology;

[0143] - Neutrazen™ (Pal-His-D-Phe-Arg-NH2) sold by the company Innovations; or

[0144] - BONT-L-Peptide™ (INCI name = Palmitoyl Hexapeptide-19: product of the reaction of palmitic acid and Hexapeptide-19 (synthetic peptide consisting of asparagine, aspartic acid, lysine and methionine), Timp-Peptide™ (INCI name = Acetyl Hexapeptide-20: product obtained by acetylation of Hexapeptide-20 (synthetic peptide consisting of alanine, glycine, lysine, valine and proline) or ECM Moduline™ (INCI name = Palmitoyl Tripeptide-28: product of the reaction of palmitic acid and Tripeptide-28 (synthetic peptide consisting of arginine, lysine and phenylalanine) sold by the company Infinitec Activos.

[0145] It is also possible to combine the invention with one or more cyclic peptides, in particular those extracted from flax seed oil described in the Applicant's patent application WO20 19 / 149450.

[0146] The sphingolipid(s) according to the invention or the composition containing them may be combined with at least one additional hair care ingredient, preferably with at least one of the compounds chosen from one or more surfactants, in particular nonionic surfactants, amphoteric surfactants and cationic surfactants, vitamin B3 compounds, compounds such as niacinamide or tocopherol, retinoid compounds such as retinol, compounds such as phytosphingosine, sphinganine or their derivatives, which may be dihydrosphingosine, dehydrosphingosine, dehydrophytosphingosine, acetylphytosphingosine or tetraacetylphytosphingosine, a ceramide other than that or those preferentially used according to the invention, in particular a ceramide AS, a ceramide AH, a ceramide AG, a ceramide AP, a ceramide NS, a ceramide NH, a ceramide NG, a ceramide NP, a ceramide OS, a ceramide OH, a ceramide OG, a ceramide OP, a ceramide EOS, a ceramide EOH, a ceramide EOG, a ceramide EOP, cholesterol, a glycosphingolipid, hexamidine, a-lipoic acid, resveratrol or DHEA, hyaluronic acid, peptides, including N-acetyl-Tyr-Arg-O-hexadecyl, Pal- VGVAPG (SEQ ID NO: 26), Pal-KTTKS (SEQ ID NO: 1), Pal-KTSKS (SEQ ID NO: 2), Pal- GQPR (SEQ ID NO: 3), Pal-PP, Pal-GHK, Pal-KMO2K and Pal-K(P)HG (MATRIXYL Morphomics™, marketed by Sederma) which are classic active ingredients used in topical cosmetic or dermo-pharmaceutical compositions.

[0147] Preferably according to the invention, the hair composition contains at least one surfactant, which may be non-ionic, amphoteric or cationic. Additional hair care ingredients may be added such as sphingosine, phytosphingosine, sphinganine or their derivatives, which may be dihydrosphingosine, dehydrosphingosine, dehydrophytosphingosine, acetylphytosphingosine or tetraacetylphytosphingosine, a ceramide other than that or those preferentially used according to the invention, in particular a ceramide AS, a ceramide AH, a ceramide AG, a ceramide AP, a ceramide NS, a ceramide NH, a ceramide NG, a ceramide NP, a ceramide OS, a ceramide OH, a ceramide OG, a ceramide OP, a ceramide EOS, a ceramide EOH, a ceramide EOG, a ceramide EOP, cholesterol, a glycosphingolipid, a peptide, in particular chosen from: N-acetyl-Tyr-Arg-O-hexadecyl, Pal-VGVAPG (SEQ ID NO: 26), Pal-KTTKS (SEQ ID NO: 1), Pal-KTSKS (SEQ ID NO: 2), Pal-GQPR (SEQ ID NO: 3), Pal-PP, Pal-GHK (rev14), Pal-KMO2K and Pal-K(P)HG.

[0148] A composition according to the invention can be applied to the face, body, decollete, scalp, hair, eyelashes, body hair, in any form or vehicle known to those skilled in the art, in particular in the form of a solution, dispersion, emulsion, paste or powder, individually or in a premix or be carried individually or in a premix by vectors such as macrocapsules, microcapsules or nanocapsules, in particular lipid ones, macrospheres, microspheres, or nanospheres, liposomes, oleosomes or chylomicrons, macroparticles, microparticles or nanoparticles, macrosponges, microsponges or nanosponges, microemulsions or nanoemulsions, sequestrants or adsorbed on powdery organic polymers, talcs, bentonites, spores or exines and other mineral or organic supports.

[0149] Hair care compositions may be in various forms, including hair conditioners, hair straightening formulations, straightening and curling products, perms, hair shampoos, preshampoo conditioners, conditioners, lotions, leave-on shampoos, styling products, leave-in hair products, waterless products, emulsions, 2-in- 1 foaming emulsions, creams, masks, aerosol or non-aerosol foams, sprayable emulsions, emulsifier-free products, aqueous or oily sprays, serums, gels, mild sulfate-free formulations, silicone-free formulations, products containing pigments, shower products or colored cosmetics such as mascaras and coloring formulations.

[0150] These hair care compositions comprising at least one sphingolipid according to the invention may comprise various ingredients known to those skilled in the art such as, for example and without being exhaustive, cleaning agents, surfactants, revitalizing agents, styling agents, anti-dandruff agents, sequestering or complexing agents (EDTA and its salts), stabilizing agents, pearlescent and opacifying agents; plasticizing or coalescing agents, gelling agents, emollient agents, acidifying or alkalizing agents, hair growth promoters, anti-hair loss agents, fragrances, essential oils, polymers, proteins or derivatized proteins, silicones, ceramides, sunscreen compounds (filters), pigments, moisturizers, antioxidants, co-emulsifiers, filmforming agents, alpha-hydroxy acids, hair colorants, detergents, thickening agents, sheathing agents, hair conditioning agents, texturizing agents, antiseptic agents, preservatives and surfactants.

[0151] A “conditioning agent” means a hair care product for revitalizing the hair by modifying the frictional and / or mechanical properties of the hair.

[0152] Conditioning agents may be applied to the hair when it is wet, for example during a shower, or when the hair is dry. Most often, the term refers to the former. Hair conditioning ingredients are generally applied from a formulation comprising the conditioning ingredients in combination with a number of lipophilic ingredients.

[0153] Hair care compositions are prepared according to methods known to those skilled in the art. The vehicle or excipient supporting the formulation may be water, oil, a powder, depending on the final destination of the formula: if for example, it is a shampoo, it may be water; for other formulations, an oil will be preferred: such as vegetable oils (coconut, argan, jojoba, olive, sunflower, etc.), mineral oils, animal or synthetic oils. Synthetic esters, such as C1215 Alkyl Benzoate, may also be used as an excipient. Liquid fatty alcohols, liquid fatty esters, solid fatty substances and in particular waxes, solid fatty esters, solid alcohols may also be used as a carrier.

[0154] The present invention covers a non-therapeutic, cosmetic topical treatment method for preserving and improving the appearance and general condition of hair, in particular for inducing and / or stimulating the growth of hair, body hair, eyelashes and eyebrows, protecting their structure, slowing their loss, preventing their depigmentation and / or inducing their pigmentation, comprising the topical application to the hair, body hair, eyelashes and / or eyebrows, in a subject in need thereof, of an effective amount of at least one sphingolipid according to the invention or of a composition comprising same, the sphingolipids being as defined above.

[0155] The present invention also provides a hair treatment method which comprises the application to the hair of a composition comprising at least one sphingolipid according to the invention and optionally, rinsing this composition. The method consists in applying an effective amount of at least one sphingolipid according to the invention to the hair and / or body hair in need thereof. The "effective" amount depends on various factors, such as age, the condition of the person, the severity of the disorder and the method of administration. An effective amount means a non-toxic amount sufficient to obtain the desired effect.

[0156] According to other features, the cosmetic treatment method according to the invention can be combined with one or more other treatment methods targeting the hair and body hair, such as for example light therapy, heat or aromatherapy treatments.

[0157] According to the invention, it is possible to propose multi-compartment devices or kits intended for implementing the method described above, and which could comprise, by way of example, and without this being limiting, in a first compartment the active ingredient according to the invention and in a second compartment an additional excipient and / or active, the compositions contained in said first and second compartments being considered here as a combination composition for simultaneous, separate or spread out use over time, in particular in one of the treatments defined above.

[0158] DETAILED DESCRIPTION

[0159] The present invention will be better understood in light of the following description of an example of embodiment and in vitro, ex vivo and in vivo tests.

[0160] 1- Example of preparation of active ingredients suitable for the treatment according to the invention

[0161] 1.1- Ingredient in powder form

[0162] The following specific mixture of fatty acids is prepared:

[0163] [Table 1]

[0164] 3.5 g of the thus prepared fatty acid mixture is dissolved in 20 ml of ethyl acetate, followed by the addition of 3 g of tosyl chloride and 1 g of DMAP, and reacted for 0.5 hour. After that, 4 g of phytosphingosine is added. After the addition of phytosphingosine, the reaction is continued for 2 hours, after which the reaction mixture is cooled to 10 degrees Celsius and filtered to obtain 4 g of white filtrate. The obtained white filtrate is dried to obtain a powder and then analyzed by liquid chromatography, confirming that 98% of the area value is attributed to the ceramide NP mixture peak and the distribution of fatty acid chains as mentioned in the table above and described in the table below is confirmed by gas chromatography. [Table 2]

[0165] This product in powder form, 98% pure in ceramides NP, with a majority of fatty acid chain length in C20 and C22, can be used as an ingredient to manufacture cosmetic formulas.

[0166] It was used in the tests below and called ("sphingolipid" according to the invention or more precisely "sphingolipid C20-C22" according to the invention).

[0167] 1.2- Ingredient in the form of a liquid solution

[0168] Approximately 0.5% of the sphingolipid according to the invention described above in point 1.1 are solubilized using a surfactant, for example steareth-20, in a matrix, for example a mixture of water and glycerin. Optionally, the composition can be preserved for example with potassium sorbate and I or chlorhexidine digluconate.

[0169] 1.3- Ingredient in the form of an emulsion

[0170] The composition described in the following table constitutes an ingredient suitable for the treatment according to the invention in that it contains the sphingolipid according to the invention. It also advantageously contains phytosphingosine as another active ingredient as well as cholesterol and two fatty acids. These additional active ingredients are very often associated with ceramides.

[0171] [Table 3]

[0172] An emulsion is formed, white in color and with a viscosity of 20,000 to 40,000 cp.

[0173] 1.4- Ingredient in oil form

[0174] This composition comprises 5% by weight of the sphingolipid according to the invention in an oil suitable for a hair cosmetic product, such as peanut, avocado, olive, argan, coconut, rosemary or sunflower oil, and an emollient to aid solubilization such as an isopropyl / isostearate ester, isopropyl / myristate, triisostearin or ethyl-hexyl-palmitate.

[0175] 2- Examples of cosmetic formulas

[0176] Different cosmetic formulations are described below, containing the sphingolipid according to the invention.

[0177] Whether used pure or diluted in a premix as described above (in the form of a liquid ingredient, emulsion or oil) to produce the formulation, the sphingolipid for the treatment according to the invention is generally recommended in a cosmetic formula at a rate of 0.01% to 5%, preferably a rate between 0.1% and 1%, more preferably at a rate of 0.1 to 0.5%. It goes without saying that these rates could vary without departing from the scope of the present invention, depending on the more or less pronounced effects sought.

[0178] Examples of formulation are described below. In the formulas described, the ingredient used is pure sphingolipid in powder form.

[0179] Additional active ingredients may support and / or complement the activity of the active ingredient according to the invention. These ingredients can be of any category depending on their function(s), the place of application (body, face, neck, bust, hands, etc.), the desired final effect and the targeted consumer.

[0180] Example 1 : Scalp lotion

[0181] [Table 4]

[0182] Procedure: Weigh and mix A. Weigh and mix B. Add B to A, stirring in a water bath. Activate A+B by stirring vigorously. Weigh and heat C, mix well. Weigh and mix D. Add C to D, mix well. Add C+D to A+B, homogenize. Add E, to A+B+C+D, mix well.

[0183] Example 2: Scalp cream

[0184] [Table 5]

[0185] Procedure: Weigh and mix A. Weigh and mix B. Add B to A, stirring in a water bath. Activate A+B by stirring vigorously. Weigh and heat C, mix well. Weigh and heat D, mix well. Add C to D, mix well. Add C+D to A+B, homogenize. Add E, to A+B+C+D, mix well.

[0186] Example 3: Hair gel

[0187] [Table 6]

[0188] Procedure: Weigh and mix A. Weigh and mix B. Add B to A, stirring in a water bath. Activate A+B by stirring vigorously. Weigh and heat C, mix well. Add C to A+B, homogenize. Weigh and mix D. Add D to A+B+C, mix well.

[0189] Example 4: Night mask

[0190] [Table 7]

[0191] Procedure: Weigh and heat A in a bain-marie. Weigh and heat B in a bain-marie. Weigh and heat C, mix well. Add C to A, while stirring. Disperse B in A+C while stirring vigorously, homogenize. Add D to A+B+C, mix well.

[0192] Example 5: Cleansing conditioner

[0193] [Table 8]

[0194] Procedure: Weigh and heat A in a water bath. Weigh and heat B in a water bath. Weigh and mix C. Add C to A, while stirring. Add B to A+C while stirring, homogenize.

[0195] Example 6: Shampoo

[0196] [Table 9]

[0197] Procedure: Weigh and heat A in a bain-marie. Weigh and heat B in a bain-marie. Weigh and heat the ingredients of C separately. Add B to A, while stirring. Add the ingredients of C one after the other to A+B while stirring, homogenize. Add D to A+B+C, homogenize. Example 7: Shampoo

[0198] [Table 10]

[0199] Procedure: Weigh and heat A in a bain-marie. Weigh and mix B. Add B to A, stirring. Weigh and heat C, mix well. Add C to A+B, stirring, homogenize. Add D to A+B+C, homogenize.

[0200] Example 8: Wax

[0201] [Table 11]

[0202] Procedure: Weigh and heat A in a bain-marie, homogenize.

[0203] Example 9: Hair serum

[0204] [Table 12]

[0205] Procedure: Weigh and heat A in a bain-marie. Weigh and mix B. Add B to A, stirring. Weigh and heat C, mix well. Add C to A+B, stirring, homogenize. Add D to A+B+C, homogenize. Example 10: Hair oil

[0206] [Table 13]

[0207] Examples of additional active ingredients for these different formulas:

[0208] Apiscalp™ (INCI: Caprylic / Capric Triglyceride (and) Apium Graveolens (Celery) Seed Extract): active ingredient marketed by Sederma, to combat itching, dryness and hyperseborrhea of the irritated scalp.

[0209] HELIOGENOL™ (INCI:

[0210] Phytolea™ Baobab EC (INCI: Adansonia Digitata Seed Oil): active ingredient sold by Crodarom, regenerating and antioxidant thanks to its content of fatty acids and vitamins E and A.

[0211] Phytolea™ Cranberry EC (INCI: Vaccinium Macrocarpon (Cranberry) Seed Oil): active ingredient moisturizing the scalp sold by Crodarom.

[0212] Ceramide HO3 (INCI: Trihydroxypalmitamidohydroxypropyl Myristyl Ether): active ingredient sold by Sederma, helps repair damaged hair and hair and promotes their hydration.

[0213] Crodabond™ CSA (INCI: Hydrogenated Castor Oil / Sebacic Acid Copolymer): active ingredient sold by Croda, which seals raised cuticles (the outermost layer of the hair shaft) and repairs split ends.

[0214] Seatons Coconut Oil (INCI: Cocos Nucifera (Coconut) Oil): active ingredient marketed by Croda, for immediate hydration of hair with a smooth and silky touch.

[0215] Hairspa™ (INCI: Glycerin (and) Lactitol (and) Xylitol): active ingredient sold by Sederma, calming and moisturizing for the scalp, based on lactitol and xylitol.

[0216] Phytessence™ Hazel Leaf (INCI: Glycerin (and) Water (and) Corylus Avellana Leaf extract): active ingredient sold by Crodarom, restoring vitality and tone to the scalp.

[0217] Crodarom® Manuka Honey (INCI: Water (and) Glycerin (and) Honey Extract) active ingredient sold by Crodarom, repairs damaged hair and hair. Matcha Tea Extract™ (INCI: Glycerin (and) Water (and) Camellia Sinensis Leaf Extract): active ingredient sold by Crodarom, antioxidant and purifying.

[0218] NG Unsaponifiable Shea Butter ™ (INCI: Butyrospermum Parkii (Shea) Butter (and) Butyrospermum Parkii (Shea) Butter Unsaponifiables): active ingredient sold by Sederma, restores the barrier function and improves hydration.

[0219] Neroli Floral Water™ (INCI I Water (and) Citrus Aurantium Amara (Bitter Orange) Flower Water): active ingredient sold by Crodarom, with calming and regenerating properties.

[0220] Procapil™ (INCI: Butylene Glycol (and) Water (and) PPG-26-Buteth-26 (and) PEG-40 Hydrogenated Castor Oil (and) Apigenin (and) Oleanolic Acid (and) Biotinoyl Tripeptide-1) active ingredient sold by Sederma, preventing hair loss.

[0221] Silverfree™ (INCI: Glycerin (and) Aqua (and) Palmitoyl-dipeptide-52): active ingredient sold by Sederma, for a long-lasting hair repigmenting effect.

[0222] Venuceane™ (INCI: Thermus Termophillus Ferment (and) Glycerin): active ingredient sold by Sederma, preventing damage caused by UV and IR radiation.

[0223] Zinc Pyrithione: anti-dandruff agent.

[0224] KeraBio™ K31 (INCI: Aqua (and) Hydrolyzed sr-(Tripeptide-137 Hexapeptide-40 sh- Polypeptide-184 sh-Polypeptide-146)): active ingredient sold by Croda, Biotech powered biomimetic bond builder with pure, potent performance. Delivers a vegan keratin recharge at the molecular level, elevating hair strength beyond repair.

[0225] FibraShield™ C (INCI: Aqua (and) Hydrolyzed Cicer Seed Extract): active ingredient sold by Croda, a protective multi-peptide that fights oxidative stress inside and out to preserve hair longevity and protects from environmental damage, maintaining hair health throughout life.

[0226] 3- In vitro studies

[0227] The tests were carried out with the pure powdered sphingolipid according to the invention described in point 1.1 above (with a fatty acid whose hydrocarbon chain is C20-C22).

[0228] 3.1- Anti-hair loss

[0229] 3.1.1- Inhibition of irritation

[0230] Protocol

[0231] HaCaT human keratinocytes are cultured until sub-confluence, then are seeded and placed in contact with the sphingolipid according to the invention and / or sodium dodecyl sulfate (abbreviated SDS) to mimic the irritant effect. After incubation, the medium is removed and the cells are washed with phosphate-buffered saline (abbreviated PBS). The cells are lysed and their RNA extracted. After quantification of RNA by NanoDrop spectrophotometry, reverse transcription followed by qPCR are performed to determine the expression levels of the genes of interest (I L-1 a, I L-1 p, IL-6, TRPV3). The data are normalized using a housekeeping gene.

[0232] 3.1.1.1- IL-1a

[0233] Results

[0234] Effect on the relative expression of IL-1 a mRNA (n=3)

[0235] [Table 14]

[0236] SDS increases I L-1 a mRNA expression. The results show that the sphingolipid according to the invention counteracts the effect of SDS by decreasing the presence of IL-1 a in cells.

[0237] 3.1.1.2- IL-1 p

[0238] Results

[0239] Effect on the relative expression of IL-1 mRNA (n=3)

[0240] [Table 15]

[0241] SDS increases I L-1 p mRNA expression. The results show that the sphingolipid according to the invention counteracts the effect of SDS by decreasing the presence of I L-1 p in cells.

[0242] 3.1.1.3- IL-6

[0243] Results

[0244] Effect on the relative expression of IL-6 mRNA (n=3)

[0245] [Table 16]

[0246] SDS increases IL-6 mRNA expression. The results show that the sphingolipid according to the invention counteracts the effect of SDS by decreasing the presence of IL-6 in cells. 3.1.1.4- TRPV3

[0247] Results

[0248] Effect on the relative expression of TRPV3 mRNA (n=3)

[0249] [Table 17]

[0250] SDS increases TRPV3 mRNA expression. The results show that the sphingolipid according to the invention counteracts the effect of SDS by reducing the presence of TRPV3 in the cells.

[0251] 3.1.1.5- Cell viability

[0252] Protocol

[0253] HaCaT human keratinocytes are cultured to sub-confluence, then seeded and placed in contact with the sphingolipid according to the invention and / or sodium dodecyl sulfate (abbreviated SDS) to mimic the irritant effect. After 24 hours of incubation, the supernatant is removed and replaced with a reagent. The absorbance is measured at 450 nm using a microplate reader.

[0254] Results

[0255] Effect on cell viability (n=3)

[0256] [Table 18]

[0257] SDS decreases cell viability. The results show that the sphingolipid according to the invention counteracts the effect of SDS on cell viability.

[0258] 3.1.2- Inhibition of oxidative stress

[0259] Protocol

[0260] HaCaT human keratinocytes are cultured to sub-confluence, then seeded and placed in contact with the sphingolipid according to the invention and / or H2O2 to mimic the effect of oxidative stress. After incubation, the medium is removed and the cells are washed with phosphate-buffered saline (abbreviated PBS). The cells are lysed and their RNA extracted. After quantification of RNA by NanoDrop spectrophotometry, reverse transcription followed by qPCR are performed to determine the expression levels of the genes of interest (IL-1 a, I L-1 p, IL-4, IL-13, TRPV3). The data are normalized using a housekeeping gene.

[0261] 3.1.2.1- IL-1a

[0262] Results

[0263] Effect on the relative expression of I L-1 a mRNA (n=3)

[0264] [Table 19]

[0265] H2O2 increases I L- 1 a mRNA expression. The results show that the sphingolipid according to the invention counteracts the effect of H2O2 by reducing the presence of I L-1 a in cells.

[0266] 3.1.2.2- IL-10

[0267] Results

[0268] Effect on the relative expression of IL-1 mRNA (n=3)

[0269] [Table 20]

[0270] H2O2 increases I L-1 p RNA expression. The results show that the sphingolipid according to the invention counteracts the effect of H2O2 by reducing the presence of I L-1 p in cells.

[0271] 3.1.2.3- IL-4

[0272] Results

[0273] Effect on the relative expression of IL-4 mRNA (n=3)

[0274] [Table 21] H2O2 increases IL-4 mRNA expression. The results show that the sphingolipid according to the invention counteracts the effect of H2O2 by reducing the presence of IL-4 in cells.

[0275] 3.1.2.4- IL-13

[0276] Results

[0277] Effect on the relative expression of IL-13 mRNA (n=3)

[0278] [Table 22]

[0279] H2O2 increases IL-13 mRNA expression. The results show that the sphingolipid according to the invention counteracts the effect of H2O2 by reducing the presence of IL-13 in cells.

[0280] 3.1.2.5- TRPV3

[0281] Results

[0282] Effect on the relative expression of TRPV3 mRNA (n=3)

[0283] [Table 23]

[0284] H2O2 increases the expression of TRPV3 mRNA. The results show that the sphingolipid according to the invention counteracts the effect of H2O2 by reducing the presence of TRPV3 in the cells.

[0285] 3.1.2.6- Cell viability

[0286] Protocol

[0287] HaCaT human keratinocytes are cultured to sub-confluence, then seeded and placed in contact with the sphingolipid according to the invention and / or H2O2 to mimic the effect of oxidative stress. After incubation, the supernatant is removed and replaced with a reagent. The absorbance is measured at 450 nm using a microplate reader. Results

[0288] Effect on cell viability (n=3)

[0289] [Table 24]

[0290] H2O2 decreases cell viability. The results show that the sphingolipid according to the invention counteracts the effect of H2O2 on cell viability.

[0291] 3.1.3- Inhibition of atopic factors

[0292] Protocol

[0293] HaCaT human keratinocytes are cultured to sub-confluence, then seeded and placed in contact with the sphingolipid according to the invention and / or TNF-a / INF-y to mimic the effect of atopic stress. After incubation, the medium is removed and the cells are washed with phosphate-buffered saline (abbreviated PBS). The cells are lysed and their RNA extracted. After quantification of RNA by NanoDrop spectrophotometry, reverse transcription followed by qPCR are performed to determine the expression levels of the genes of interest (IL-1a, IL-8 or TARC). The data are normalized using a housekeeping gene.

[0294] 3.1.3.1- IL-1a

[0295] Results

[0296] Effect on the relative expression of IL-1 a mRNA (n=3)

[0297] [Table 25] F-y increases IL-1 a mRNA expression. The results show that the sphingolipid according to the invention can counteract the effect of TNF-a / INF-y by reducing the presence of I L-1 a in cells. 3.1.3.2- IL-8

[0298] Results

[0299] Effect on the relative expression of IL-8 mRNA (n=3)

[0300] [Table 26] F-y increases IL-8 mRNA expression. The results show that the sphingolipid according to the invention can counteract the effect of TNF-a / INF-y by decreasing the presence of IL-8 in cells.

[0301] 3.1.3.3- TARC

[0302] Results

[0303] Effect on relative TARC mRNA expression (n=3)

[0304] [Table 27] F-y increases the expression of TARC mRNA. The results show that the sphingolipid according to the invention counteracts the effect of TNF-a I INF-y by reducing the presence of TARC in the cells.

[0305] 3.1.4- Conclusion

[0306] The treatment according to the invention using a sphingolipid reduces scalp irritation, to soothe it and make it more comfortable. It also reduces the harmful effects of oxidative stress and reduces inflammatory factors related to atopic dermatitis. All these effects allow the scalp to be in a healthy environment for the hair, more particularly for the hair follicles which are better anchored in this scalp, and to reduce hair loss. 3.2- Hair growth

[0307] 3.2.1- Proliferation of HFDPCs

[0308] Protocol

[0309] HFDPCs are seeded in their growth medium. After 24 hours of incubation, the sphingolipid according to the invention is placed in contact with the cells for 72 hours. The cells are rinsed with a PBS solution and treated with a reagent. The measurements are carried out at 450 nm using a microplate reader spectrophotometer. Two sphingolipids according to the invention are tested, the first corresponding to that described in point 1.1 (ceramide having the fatty acid part with a hydrocarbon chain mainly in C20-C22 and the second an identical ceramide but having the fatty acid part with a hydrocarbon chain of the Oleyl type (essentially in C18).

[0310] Results

[0311] Effect on the proliferation of HFDPC cells compared to the control (n=3)

[0312] [Table 28]

[0313] The effect on the increase in the proliferation of HFDPC cells of C20-22 ceramide is significantly greater than C18 ceramide by +13.43%.

[0314] 3.2.2. Expression of key genes related to hair shaft growth

[0315] Protocol

[0316] HFDPCs are seeded in their growth medium. After 24 hours, a purge is carried out in serum- free medium, then the sphingolipid according to the invention in C20-C22. Minoxidil is brought into contact for 24 hours. Minoxidil serves as a reference for hair growth. At the end of this contact, the cells are lysed and their RNA extracted. After quantification of the RNA by NanoDrop spectrophotometry, reverse transcription followed by qPCR are carried out to determine the expression levels of the genes of interest (FGF7 and Noggin). Data are normalized using a housekeeping gene. 3.2.2.1- FGF7

[0317] Results

[0318] Effect of the sphingolipid according to the invention on the expression of the FGF7 gene compared to a negative control or a Minoxidil control (n=3)

[0319] [Table 29]

[0320] The results show that the C20-C22 sphingolipid increases the expression of the FGF7 gene which is synthesized by HFDPCs cells. This gene promotes the proliferation of HFDPCs as well as hair follicle stem cells.

[0321] 3.2.2.2- Noggin

[0322] Results

[0323] Effect of the sphingolipid according to the invention in C20-C22 on the expression of the

[0324] Noggin gene compared to a negative control or a Minoxidil control (n=3)

[0325] [Table 30]

[0326] The results show that the C20-C22 sphingolipid according to the invention increases the expression of the Noggin gene which is synthesized by HFDPC cells. This gene stimulates the induction of the hair follicle.

[0327] 3.2.3- Conclusion

[0328] The treatment according to the invention using a sphingolipid increases the cell proliferation of HFDPCs as well as the expression of genes related to hair growth, thus increasing the density and growth of hair fibers. 4- Ex vivo studies on scalp improvement

[0329] The studies were carried out with a cream according to the invention containing 0.5% by weight of pure sphingolipid in powder form and as prepared in point 1.1 above, or a placebo cream not containing said sphingolipid.

[0330] Protocol

[0331] A reconstituted epidermis model is treated with an SDS solution for 1 hour, then washed with PBS. The model is then placed in contact with the cream according to the invention or the placebo cream (control case). Immunofluorescence staining is carried out after 48 hours of contact. Antibodies against filaggrin, involucrin and loricrin were used. The observation was made using a fluorescence microscope.

[0332] 4.1- Filaggrin

[0333] Results

[0334] Effect of a cream according to the invention on the relative intensity of filaggrin compared to the SDS control (n=3)

[0335] [Table 31]

[0336] The results show that the cream according to the invention increases filaggrin, which is decreased by SDS.

[0337] 4.2- Involucrin

[0338] Results

[0339] Effect of a cream according to the invention on the relative intensity of involucrin compared to the SDS control (n=3)

[0340] [Table 32]

[0341] The results show that the cream containing the ingredient according to the invention increases involucrin, which is decreased by SDS. 4.3- Loricrin

[0342] Results

[0343] Effect of a cream containing the ingredient according to the invention on the relative intensity of loricrin compared to the SDS control (n=3)

[0344] [Table 33]

[0345] The results show that the cream containing the ingredient according to the invention increases loricrin, which is decreased by SDS.

[0346] 4.4- IL-1 a

[0347] Protocol

[0348] The skin model was treated with an SDS solution for 1 hour, then washed with PBS. The skin model is then placed in contact with a cream containing the ingredient according to the invention or not (control case). The supernatants were recovered, centrifuged and used for the measurement of the concentration of IL-1 a by the ELISA method.

[0349] Results

[0350] Effect of a cream containing the ingredient according to the invention on the relative expression of IL- 1a compared to the SDS control (n = 3)

[0351] [Table 34]

[0352] The results show that the cream containing the ingredient according to the invention significantly reduces the presence of I L-1 a in skin cells, which is increased by SDS.

[0353] 4.5- Aquaporin-3

[0354] Protocol

[0355] A skin model is treated with an SDS solution for 1 hour, then washed with PBS. The skin model is then placed in contact with a cream containing the ingredient according to the invention or not (control case) for 24 hours. At the end of this contact, the cells are lysed and their RNA is extracted. After quantification of the RNA by NanoDrop spectrophotometry, reverse transcription followed by qPCR are performed to determine the expression levels of the gene coding for aquaporin-3. The data are normalized using a housekeeping gene.

[0356] Results

[0357] Effect of a cream containing the ingredient according to the invention on the relative expression of aquaporin-3 mRNA compared to the SDS control (n=3)

[0358] [Table 35]

[0359] The results show that the cream containing the ingredient according to the invention increases the gene expression of aquaporin-3, which is decreased by SDS.

[0360] 4.6- Conclusion

[0361] All these results show that the ingredient according to the invention repairs the skin barrier damaged by the use of irritating products, making it possible to obtain a healthier scalp favorable to the anchoring of hair follicles and hair growth.

[0362] 5- Ex-vivo studies on strands of hair

[0363] Protocol

[0364] The study on the hair was carried out by applying the hair oil according to the invention described above in example 10 in the examples of cosmetic formulas section. This oil contains 0.5% of sphingolipid according to the invention. Four studies were carried out for a total of 80 strands of hair (40 undamaged strands and 40 strands of damaged hair). Each group of hair strands was divided into two groups: 20 strands receiving the placebo oil and 20 strands receiving the oil according to the invention. Each hair strand was washed with a diluted SDS solution. The four studies were carried out before and immediately after the application of the oil, as reported in the table below.

[0365] [Table 36]

[0366] DSLR (digital single-lens reflex): photography using a digital SLR camera ** SEM: scanning electron microscopy

[0367] All measurements were carried out in a room at constant temperature (20-22 °C) and humidity (40-60%).

[0368] The results were compared:

[0369] - before and after application of the oil according to the invention; and

[0370] - after application, between the oil according to the invention and the placebo oil, i.e. which contains the same ingredients in the same quantity, except for the active ingredient according to the invention.

[0371] Various statistical tests were used:

[0372] [Table 37]

[0373] The results are significant if p<0.05.

[0374] 5.1- Hydration

[0375] Protocol

[0376] The moisture content of the hair was measured using the HX204 halogen moisture analyzer (Mettler Toledo). It is equipped with a halogen lamp and a temperature sensor, which can quickly heat the internal temperature and quantify the moisture content by measuring the change in the weight of the product. The moisture content of the hair (%) was calculated by the difference in the weight of the hair before and after drying. The higher measurement shows the increase in hair hydration.

[0377] Results

[0378] Effect of the oil according to the invention on hair hydration

[0379] [Table 38]

[0380] The results show that after applying the oil according to the invention, hair hydration is significantly improved. The placebo oil, however, had no significant effect on hair hydration.

[0381] In addition, the oil according to the invention significantly improves hair hydration compared to the placebo oil.

[0382] 5.2- Shine

[0383] Protocol

[0384] Images are acquired using a digital SLR camera (DSLR). These photos are standardized: they are acquired by the same researcher, in identical lighting conditions, with photography conditions (direction and location of the measurement) fixed using equipment. The images are acquired with a shiny band on the hair. The image analysis is carried out by a special program (Image-Pro Plus, USA) which records several hue and saturation values for the shiny band (denoted SB) and for the black band (denoted BB). The ratio is calculated by the ratio between the values of the bands. The highest ratio shows the increase in hair shine.

[0385] Results

[0386] Effect of the oil according to the invention on hair shine

[0387] [Table 39]

[0388] The results show that after the application of the oil according to the invention, the shine of the hair is significantly improved and superior to the placebo oil.

[0389] 5.3- Detangling

[0390] Protocol

[0391] The strand of hair is combed downwards from the starting point, until the hair becomes tangled in the comb. The distance is measured in cm. An increase in the value of the length (cm) indicates an improvement in the detangling of the hair Results

[0392] Effect of the oil according to the invention on the detangling of the hair

[0393] [Table 40]

[0394] The results show that after the application of the oil according to the invention, the shine of the hair is significantly improved and superior to the placebo oil.

[0395] 5.4- Roughness / Softness

[0396] Protocol

[0397] Hairs from the hair strands are randomly selected in each group. Images are acquired using a scanning electron microscope (SEM, Teneo VS™, ThermoFisher). The image analysis is carried out by a special program (Image-Pro Plus, USA) to analyze the damaged areas (pixel). The decrease in the number of pixels shows the repair of the damaged hair cuticles (reduction of roughness).

[0398] Results

[0399] Effect of the oil according to the invention on hair roughness

[0400] [Table 41]

[0401] The results show that after applying the oil according to the invention, the roughness of the hair is significantly reduced. The placebo oil, however, had no significant effect on roughness. In addition, the oil according to the invention significantly reduces the roughness of the hair compared to the placebo oil. 5.5- Conclusion

[0402] All these results show that the treatment according to the invention allows you to have beautiful hair, more hydrated, shinier, less rough and therefore softer and easier to detangle

[0403] 6- In vivo study on the scalp

[0404] Protocol

[0405] The in vivo study on the scalp was carried out by applying a hair lotion according to the invention described above in example 9 in the examples of cosmetic formulas section.

[0406] Three studies were conducted for a total of 44 female volunteers aged between 26 and 58 (average age: 49). Volunteers were divided into two groups: 22 women received the placebo lotion and 22 women received the lotion according to the invention.

[0407] All volunteers were asked to wash and dry their hair the evening before the first visit and to stop using hair products (rinse, treatment, hair oil, hair mask, essence, etc.) on the test site (scalp) at least 12 hours before the visit. In addition, volunteers were asked not to use the same or similar product during the two weeks of the study. All three studies were performed before and immediately after application of the product, as reported in the table below.

[0408] [Table 42]

[0409] * measurements explained later

[0410] All measurements were carried out in a room at constant temperature (20-22°C) and humidity (40-60%). The volunteers remained in this room for 30 minutes before the measurements.

[0411] The results were compared:

[0412] - before and after application of the lotion according to the invention; and

[0413] - after application, between the lotion according to the invention and the placebo lotion, i.e. which contains the same ingredients in the same quantity, except for the active ingredient according to the invention (sphingolipid).

[0414] Different statistical tests were used: [Table 43]

[0415] The results are significant if p<0.05.

[0416] 6.1- Soothing

[0417] Protocol

[0418] Images of the scalp temperature are acquired using the R300S infrared thermal camera. These photos are standardized: they are acquired at a constant angle and distance over time. The temperature is expressed in degrees Celsius (°C), and a decrease in the value means that the scalp is soothed.

[0419] Results

[0420] Effect of the lotion according to the invention on the scalp temperature.

[0421] [Table 44]

[0422] The results show that after application of the lotion according to the invention, the temperature of the scalp is significantly reduced, and more significantly than for the placebo lotion.

[0423] 6.2- Hydration

[0424] Protocol

[0425] Scalp hydration was evaluated using the DermaLab® which is a device particularly suited to measuring hydration on the scalp due to the structure of its probe equipped with 86mm pins allowing on the one hand better access to the scalp and on the other hand to reduce the accumulation of water on the probe. The measurement was carried out 3 times. The scalp hydration unit is expressed in microsiemens (pS), and an increase in the measurement value means an improvement in scalp hydration.

[0426] Results

[0427] Effect of the lotion according to the invention on scalp hydration

[0428] [Table 45]

[0429] The results show that after application of the lotion according to the invention, scalp hydration is significantly increased. The placebo lotion, however, had no significant effect on scalp hydration.

[0430] In addition, the lotion according to the invention significantly increases scalp hydration compared to the placebo lotion.

[0431] 6.3- Desquamation

[0432] Protocol

[0433] A scalp sample was taken from the scalp using a black D-Squame™ adhesive tape. Images are acquired using an iScope™ device (MORITEX) capable of x700 magnification.

[0434] The image analysis is carried out by a special program (Image-Pro Plus™, USA) to evaluate scalp desquamation.

[0435] Results

[0436] Effect of the lotion according to the invention on scalp desquamation

[0437] [Table 46]

[0438] The results show that after applying the lotion according to the invention, scalp flaking is significantly reduced and more significantly compared to the placebo lotion. 6.4- Conclusion

[0439] All these results show that thanks to the treatment according to the invention, the scalp is more soothed, more hydrated and flakes less. This provides an environment favorable to the anchoring of hair follicles and growth of the hair shaft in better conditions.

[0440] 7- Ex-vivo evaluation of protective effects on the hair cortex following thermal exposure of hair fibres (Flat iron)

[0441] Sphingolipids, in particular ceramides, are essential structural lipids naturally present within the hair fibre, forming part of the cell membrane complex (CMC) that acts as the “cement” between cuticle and cortex cells. This complex ensures the cohesion and integrity of the hair shaft, protecting it against physical, chemical, and thermal damage.

[0442] Within the fibre, ceramides contribute to a protective lipid barrier that minimizes moisture loss and shields hair from environmental and heat-induced stress. This barrier limits dehydration, structural disorder, and breakage; effects that are often intensified by repeated thermal styling such as blow drying or straightening. Conversely, depletion of these lipids through aging, heat exposure, or chemical treatments leads to weaker, more brittle hair with reduced thermal resistance and smoothness.

[0443] Importantly, hair growth and ceramide levels are interconnected. Healthy, active hair follicles produce new fibres rich in structural lipids, including ceramides, which maintain internal cohesion and resilience. In contrast, when hair growth slows or excessive shedding occurs, the overall proportion of young, ceramide-rich fibres decreases, leading to diminished lipid content in the hair mass.

[0444] Thus, promoting hair growth and reducing hair loss, together with replenishing ceramides, helps maintain an optimal lipid profile within the fibre supporting structural integrity and enhancing resistance to heat-induced damage.

[0445] The test formulations used for this evaluation are disclosed in the following Table 47.

[0446] The formulation according to the invention comprises 0.2% wt. of pure sphingolipid of the invention in powder form (corresponding to the ingredient prepared at point 1.1 above).

[0447] The Placebo formulation comprises the same chassis formulation as the formulation of the invention but does not comprise the sphingolipid according to the invention. [Table 47]

[0448] A global shampoo formulation as disclosed in following Table 48 was used to wash the hair samples before heat treatment (as explained below). [Table 48]

[0449] Preparation of hair samples and heat treatment

[0450] Fine-density, dark brown, virgin European hair (18 cm in length excluding binding) was purchased from International Hair Importers & Products Inc. (Glendale, NY, USA). Hair was cut into 1.5 cm wide tresses (approximately 2 g net weight, excluding binding). The hair tresses were washed twice with the global shampoo disclosed in Table XX above (0.1 g of shampoo per g of hair). Then 0.15 g of the test formulation per g of hair was applied to each tress in the damp state. The tresses were left to air-dry overnight at room temperature (23°C ± 2°C, 45% ± 5% RH). Each tress was heat-treated with a flat iron set to 450°F for 60 seconds (10 passes, 6 seconds each) in a vertical motion starting from the top and ending at the bottom. The tresses were allowed to cool for 10 minutes at room temperature, completing 1 cycle consisting of heating followed by cooling. Each tress subsequently underwent 3 additional cycles, for a total of 4 thermal exposure cycles, equivalent to 4 minutes or 40 passes with the hot flat iron.

[0451] Testing procedure and analysis of heat-treated hair tresses

[0452] For each tress evaluated, 100 mg of hair was cut from the treated tress into approximately 2 mm snippets. The snippets were stored and equilibrated at 45% RH overnight. Next, 5- 7 mg of hair snippets were weighed into large-volume pressure-resistant stainless-steel pans. Fifty microliters (50 pL) of deionized water were added to each pan using a micropipette. The pans were sealed and stored overnight for equilibration at 45% RH. Three pans were prepared for each treatment evaluation. Samples were analysed using a TA Instruments DSC 250 Differential Scanning Calorimeter under the following conditions:

[0453] Temperature range: 50°C to 200°C

[0454] Heat rate: 10°C / min

[0455] Instrument software was used to record the denaturation temperature (TD) and denaturation enthalpy (AHD) for all three samples per treatment.

[0456] The denaturation temperature (TD) is the peak location that is related to properties of the matrix and its viscosity and is kinetically controlled by the cross-link density of the hair matrix.

[0457] The denaturation enthalpy (AHD) corresponds to the peak area that is associated with thermal stability and structural integrity of a-helical filaments.

[0458] Studies have shown that hair matrix damages result in a decrease of TD, meaning the lower the denaturation temperature, the more damaged the hair is.

[0459] The percent protection of the treated hair samples, relative to the untreated heated hair, were calculated according to the following equation (I), wherein Value represents the measured parameter (TDorAHD):

[0460] Protection (%) = ((Value treated - Value heated) I (Value unexposed - Value heated)) x 100

[0461] (I)

[0462] Results and Discussion

[0463] [Table 49]

[0464] The 0.2% wt. invention formulation exhibited superior protective effect, nearly restoring the thermal properties to unexposed hair levels, with a Toof 148.80 ± 0.29 °C and AH of 12.64 ± 1.50 J / g, corresponding to 60.4% and 98.8% recovery, respectively.

[0465] These results demonstrate that the invention formulation effectively inhibit heat-induced denaturation of hair keratin and therefore promotes hair integrity, while reducing hair loss and favouring hair growth.

[0466] 8- Ex-vivo evaluation of hair surface repair / smoothness after UV-induced damage

[0467] The condition of the hair is often inherently linked with its sensory feel, as consumers perceive that hair that feels smoother is in better condition than damaged hair, which can feel coarser. The surface friction of dry hair tresses was evaluated using a Dia-Stron MTT175 Miniature Tensile Tester. This instrument measures the dry frictional force between a hair tress and the rubber probe that mimics human skin surface. The lower the friction force, the better the hair surface smoothness, and in turn, the more chance for a consumer to perceive the touchable silky feel of the hair. To effectively improve dry state conditioning of hair, the conditioning agent must exhibit a natural tendency to “slip” in order to reduce friction force when consumers touch their hair. However, traditional conditioning agents that give positive conditioning performance in the wet state, such as quats, do not tend to show the same conditioning performance in the dry state due to the absence of water that serves as the lubricant. With the enhanced need for pleasant sensory aesthetics, the dry state condition of the hair has become increasingly important with consumers.

[0468] The same formulations as disclosed in Table 47 above were used for this evaluation, with an additional tested invention formulation identical to the invention formulation of Table 47 but comprising 0.5% wt. of pure sphingolipid of the invention in powder form.

[0469] Protocol

[0470] For this experiment, regular bleached medium-density European hair (19 cm in length, excluding binding) was purchased from International Hair Importers & Products Inc. (IHIP). Hair was cut into 1.5 cm wide tresses (approximately 3g net weight, excluding binding). Three tresses per treatment were prepared. Hair tresses were washed once with the global shampoo (0.1g shampoo / g of hair) and air-dried overnight at room temperature. Untreated dry hair friction baseline readings were obtained using a Dia-Stron MTT175 equipped with a rubber substrate and 400g brass weights, operated at a rate of 600 mm / min. Five readings were taken on each side of the hair tress, for a total of 10 readings per tress. Tresses were treated in the damp state with 0.15g of test formulation / g of hair and air-dried overnight at 23°C ± 2°C, 45% ± 5% relative humidity. To further exacerbate the efficacy of the sphingolipid, the tresses were exposed to UV irradiation by mounting them onto a rotating rack inside an Atlas Ci5000 Weather-Ometer. The Weather-Ometer conditions were as follows: a broad-band irradiance of 300 - 400 nm, UV intensity of 50 w / m2, temperature of 40°C, and a relative humidity of 65% for 3 hours per side. Each treatment cycle consisted of one wash with global shampoo, application of the formulation in the damp state, and three hours of UV exposure per side of the tress in the dry state. Subsequently, nine additional cycles were completed, and dry friction readings were obtained after the tenth cycle. Results were reported as the average horizontal force (gmf) and work done (J) from thirty measurements across three tresses. A two-tailed t-test (95% confidence level) was conducted to determine statistically significant differences in dry horizontal frictional forces and work done between baseline readings and those obtained after ten cycles of UV irradiation.

[0471] Results and discussion:

[0472] [Table 50]: Mean horizontal force (gmf)

[0473] [Table 51]: Mean work done (J) The invention formulations produced significant reductions in both frictional force and work done, indicating the strongest hair surface repair and smoothing effect from a rinse-off application on damaged and UV-exposed hair.

[0474] The placebo formulation exhibited only a minor, statistically non-significant decrease in frictional parameters.

[0475] 9- Ex-vivo evaluation for strengthening hair fibres after UV-induced stress

[0476] Cyclic fatigue testing assesses the overall influence of mechanical impact on hair and gives an indication of hair strength and surface condition. The mechanism consists of extending a certain stress onto the hair and then relaxing it. Due to the mechanism of extending a certain stress onto the hair fibre and then relaxing it, with a damage therefore progressive and localised, this constant motion of force extension and relaxation stimulates everyday styling and grooming practices. Each hair fibre is subjected to a fixed strain within the elastic region at a regular frequency. The result from the cyclic fatigue test is to measure how many times the deformation can be applied before the fibre breaks. Two parameters are measured to assess the overall dynamic strength of hair fibre:

[0477] Characteristic life (a): defined as the time when 63.2% of hair fibres have failed. An increase of characteristic life would indicate that the hair fibre is more resilient.

[0478] Survival probability: is the likelihood of hair fibres surviving x-number of cycles. A higher survival probability suggests a higher number of cycles before the point of breakage, therefore implying that the hair is stronger

[0479] After the completion of the above-mentioned smoothness evaluation of point 8 above, fifty individual hair fibres were randomly extracted from each tress previously used in the smoothness study on regular bleached and UV-irradiated hair. Each fibre measuring 30 mm in length was crimped using an AAS 1600 instrument. Prior to testing, the samples were equilibrated at 50% relative humidity in a controlled environment chamber for two hours. Cyclic fatigue testing was then conducted under constant stress mode, using the following parameters:

[0480] Target Stress: 120 MPa

[0481] Strain Rate: 40 mm / sec

[0482] Break Threshold: 15 gmf Load Position: 28 mm Maximum Cycles: 300,000

[0483] The target stress was determined by first acquiring fibre dimensions from a small batch of untreated hair and calculating the stress corresponding to the limit of elastic extension based on tensile S-N curve. Each fibre was extended to reach the target stress / load and subsequently returned to the initial load position. For each cycle, zero strain was defined at the initial load position. Upon completion of the cyclic fatigue test, each fibre was manually inspected. Any sample showing a break within 1 mm of the brass crimp was excluded from analysis, as the edge of the crimp may have interfered with the fibre, introducing a structural weakness prior to or during testing. Statistically significant differences among treatments were evaluated using Kaplan-Meier estimator with a log-rank test at 95% confidence level. Weibull analysis was also performed to model the survival probability of treated fibres, utilizing the built-in functionality of UvWin software. All previously discarded samples were excluded from the Weibull analysis.

[0484] Weibull equation (II) is as follows:

[0485] Where F(x) represents the probability of survival after x cycles. The parameter a denotes the characteristic lifetime at which 63.2% of the fibres have failed. The parameter p is the Weibull shape parameter which describes the distribution of failure rates with <1 indicating failure rate decreases with time, p =1 representing a failure rate that is constant, and p >1, indicating an increasing failure rate with time.

[0486] Results and Discussion

[0487] [Table 52]:

[0488] Significant results (p < 0.05) are denoted with asterisks

[0489] UV irradiation significantly reduced hair fibre strength in untreated samples, confirming successful induction of photodamage. Treatment with 0.2% and 0.5% invention formulations significantly increased the characteristic life (a) of hair fibers versus placebo formulation and UV-damaged untreated samples. The 0.5% invention formulation exhibited the greatest strengthening effect, improving a by +218.9% versus untreated UV and +163.8% versus placebo, with p < 0.001 in both comparisons.

[0490] By showing that hair strength is improved, it is demonstrated that a healthier hair with a better ceramide shielding is obtained thanks to the treatment with the sphingolipid of the invention.

[0491] The sphingolipid of the invention is thus advantageously also capable of improving the hair growth in the sense that hair fiber that is healthier will grow, and consequently with such healthier hair fibers hair loss will be prevented.

[0492] 10- Action of the sphingolipid of the invention on scalp microbiome

[0493] Sphingolipid of the invention used for the experiments: powder ingredient prepared according to point 1.1 above.

[0494] 1) Action on C.acnes / S. epidermis ratio a) Action on S.epidermidis growth

[0495] S.epidermidis is inoculated into its growth medium supplemented with 0.8% DMSO (solvent control) or with 4 or 8 ppm of the sphingolipid. The culture is incubated at 37°C under stirring, and the optical density at 600 nm (OD600 nm) is measured.

[0496] [Table 53]: Effect of the sphingolipid according to the invention on S. epidermidis growth at 8h of culture. The above results of Table 53 show that the sphingolipid of the invention significantly increases the growth of S. epidermidis at 4 and 8 ppm. b) Action on C.acnes growth

[0497] C. acnes is inoculated into its growth medium supplemented with 0.8% DMSO (solvent control) or with 4 and 8 ppm of the sphingolipid of the invention. The culture is incubated at 37°C under anaerobic conditions, and the optical density at 600nm (OD600nm) is measured.

[0498] [Table 54]: Effect of the sphingolipid according to the invention on C. acnes growth at 44h of culture.

[0499] The above results of Table 54 show that the sphingolipid of the invention significantly decreases the growth of C.acnes at 4 ppm and 8 ppm.

[0500] Conclusion:

[0501] By stimulating the growth of S. epidermidis and decreasing the growth of C. acnes, the sphingolipid of the invention helps restoring a more balanced ratio of C.acnes / S. epidermidis.

[0502] Sensitive scalp conditions are associated with an increased ratio of C. acnes to

[0503] S. epidermidis. By promoting the growth of S. epidermidis and inhibiting C. acnes, the sphingolipid of the invention helps restoring microbial balance, thereby alleviating symptoms linked to sensitive scalp.

[0504] Such modulation of the scalp microbiota thanks to the sphingolipid of the invention helps to strengthen the protective microbial barrier against pathogens, and may, by reducing the prevalence of C.acnes, indirectly influence sebum production, sensitive scalp being also known to be associated with excessive sebum production.

[0505] 2) Action of the sphingolipid of the invention on the growth of S. aureus

[0506] S. aureus is inoculated into its growth medium supplemented with 0.8% DMSO (solvent control) or with 8 ppm of the sphingolipid of the invention. The culture is incubated at 37°C under stirring, and the optical density at 600 nm (OD600 nm) is measured. [Table 55]: Effect of the sphingolipid according to the invention on S. aureus growth at 20h of culture.

[0507] The above results of Table 55 show that at 8 ppm, the sphingolipid of the invention decreases the growth of S. aureus by approximately 9%.

[0508] S. aureus is known to contribute significantly to scalp irritation and the development of sensitive scalp conditions. Therefore, reducing its proliferation may help alleviate the symptoms and improve scalp health.

[0509] 3) Study of the production of lipidic droplets of sebocytes after culture with or without C. acnes.

[0510] Human sebocytes derived from iPSCs (induced pluripotent stem cells) are seeded and cultured in their culture medium at 37°C, 95% humidity, and 5% CO2. In parallel, a preculture of C. acnes is done.

[0511] When the sebocytes reached 100% confluence, they are treated with the sphingolipid of the invention alone or with said sphingolipid and C. acnes. Lipid production is then studied using Bodipy staining and the expression of the lipogenesis-associated gene Plin 2 is measured using RT-qPCR.,

[0512] [Table 56]: Effect of the sphingolipid of the invention on sebum production by sebocytes

[0513] Experimental data of Table 56 demonstrate that the administration of the sphingolipid of the invention at a concentration of 8 ppm, when applied independently, results in an approximate 8% reduction in lipid droplet production. [Table 57]: Effect of the sphingolipid on sebum production by sebocytes cultivated in presence of C. acnes

[0514] In the presence of C. acnes, treatment with 8 ppm of the sphingolipid of the invention for 24 hours results in a 19% reduction in fluorescence intensity, indicating a decrease in lipid droplet accumulation.

[0515] Collectively, these findings demonstrate that the sphingolipid of the invention effectively counteracts sebum production in sebocytes, both in the presence and absence of C. acnes.

[0516] 4) Study of the expression of the Plin 2 gene of sebocytes

[0517] Human sebocytes derived from iPSCs (induced pluripotent stem cells) are cultured as described earlier. Then, cells are lysed, and their RNA is extracted. RNA quantification is performed using NanoDrop spectrophotometer, followed by reverse transcription (RT) and quantitative PCR (qPCR) to assess the expression level of Plin 2 gene. Data are normalized using a housekeeping gene.

[0518] [Table 58]: Effect of the sphingolipid of the invention on the expression of the Plin 2 gene in sebocytes

[0519] These data show that the administration of the sphingolipid of the invention at a concentration of 4 ppm and 8 ppm, results in a down regulation of Plin 2 coding gene in sebocytes. [Table 59]: Effect of the sphingolipid of the invention on the expression of the Plin 2 gene in sebocytes co-cultured with C. acnes

[0520] The treatment with the sphingolipid of the invention at a concentration of 4 ppm leads to a reduced expression of the Plin2 gene in sebocytes cultured in the presence of C. acnes.

[0521] Conclusion

[0522] Collectively, these findings demonstrate that the sphingolipid of the invention significantly downregulates the expression of Plin2, a key gene involved in lipid droplet formation. This molecular effect aligns with the observed reduction in sebum production upon sphingolipid treatment. By modulating sebum synthesis, the sphingolipid exhibits a potential benefit, particularly in conditions such as sensitive scalp, which are characterized by excessive sebum production. Thus, the sphingolipid of the invention may help restore balance and alleviate symptoms associated with sensitive scalp.

[0523] 5) Conclusion of the action of the sphingolipid of the invention on hair growth via an action on the scalp microbiome

[0524] All these results show that the sphingolipid of the invention contributes to maintaining a balanced scalp microbiota by preserving the C. acnes to S. epidermidis ratio and inhibiting the growth of S. aureus. Additionally, the sphingolipid reduces lipid production in sebocytes, both in the presence and absence of C. acnes. This reduction is evidenced at the molecular level, through downregulation of Plin2 gene expression, and at the biosynthetic level, via decreased lipid droplet formation. Through these combined actions, the sphingolipid of the invention helps prevent the onset of sensitive scalp conditions which are associated with excess sebum and microbial imbalance and thereby contribute to reducing hair loss.

Claims

Claims1. Use of at least one sphingolipid for a non-therapeutic topical cosmetic hair treatment to induce hair growth and / or slow down hair loss.

2. Use according to claim 1, wherein the sphingolipid comprises a fatty acid part with a chain that comprises from 16 to 24 carbon atoms.

3. Use according to claim 1 or 2, wherein the sphingolipid comprises a phytosphingosine as the sphingoid base.

4. Use according to one of claims 1 to 3, wherein the sphingolipid is a ceramide.

5. Use according to claim 1, wherein the ceramide corresponds to the following general formula 1:in which:R1 is -CH2-CH2-, -CH=CH- or -C(H)OH-CH2-;R2 is an alkyl, alkenyl or alkynyl chain, having from 10 to 20 carbon atoms, which may be linear or branched;-CO-R3 is a fatty acid chain having from 12 to 28 carbon atoms, R3 being an alkyl, alkenyl or alkynyl chain, which may be linear or branched, and optionally substituted by a hydroxyl group; andR4 is H or an alkyl, alkenyl or alkynyl chain, having from 1 to 10 carbon atoms; or an acylated or dehydrogenated derivative of this ceramide.

6. Use according to claim 5, wherein R1 is -C(H)OH-CH2-.

7. Use according to claim 5 or 6, wherein R4 is H.

8. Use according to one of claims 5 to 7, wherein the sphingoid base of the ceramide is phytosphingosine (corresponding to R1 = -C(H)OH-CH2-; R4 = H and R2 = C13H25).

9. Use according to one of claims 5 to 8, wherein -C0-R3 is a fatty acid chain of 16 to 24 carbon atoms.

10. Use according to claim 9, wherein -CO-R3 is a fatty acid chain of 18, 20 and 22 carbon atoms.

11. Topical use according to any one of the preceding claims of a mixture of sphingolipids which is composed of ceramides which have:- a phytosphingosine as sphingoid base; and- a fatty acid portion having at least 70% of a chain with 20 and / or 22 carbon atoms.

12. Use according to one of the preceding claims, wherein the hair treatment is further acting on the scalp and / or on the hair itself.

13. Use according to claim 12, wherein the treatment is increasing the hydration, shine, softness of the hair and ease of detangling.

14. Use according to any one of the preceding claims, wherein the treatment is improving the anchoring of the hair follicles in the scalp and improving the barrier function of the scalp.

15. Use according to any one of the preceding claims, wherein the treatment is soothing, moisturizing, and / or reducing flaking of the scalp.

16. Use according to any one of the preceding claims, wherein the treatment has an effect on the scalp microbiome.

17. Use according to any one of the preceding claims, wherein the treatment has an effect on sebum production.

18. Use according to any one of the preceding claims, wherein the treatment has a protective effect on the hair cortex following thermal exposure of hair fibres.

19. Use according to any one of the preceding claims, wherein the treatment has a hair surface repair effect and strengthening hair fibres effect after UV-induced stress.

20. Use according to any one of the preceding claims, characterized in that the at least one sphingolipid is associated with at least one additional active ingredient that can be chosen from sphingosine, phytosphingosine, sphinganine or their derivatives, an additional ceramide, cholesterol, a glycosphingolipid and / or a peptide.

21. Hair composition for a treatment according to one of the preceding claims comprising:- a mixture of ceramides whose carbon chain of the fatty acid part comprises from 16 to 24 carbons; and- a physiologically acceptable excipient comprising at least one surfactant.

22. Composition according to claim 21 , characterized in that the carbon chain of the fatty acid part comprises at least 70% of a 20 and 22 carbon chain and a phytosphingosine as sphingoid base.

23. Composition according to claim 21 or 22, consisting of a shampoo or a hair care product to be rinsed or not.

24. Composition according to one of claims 21 to 23 comprising an additional active ingredient chosen from sphingosine, phytosphingosine, sphinganine or their derivatives, an additional ceramide, cholesterol, a glycosphingolipid and / or a peptide.