Actives extractives

CRYOCARE®

Biomimetic Shield Against Thermal Stress

𝐅𝐫𝐨𝐦 𝐟𝐫𝐞𝐞𝐳𝐢𝐧𝐠 𝐚𝐢𝐫 𝐭𝐨 𝐢𝐧𝐟𝐫𝐚𝐫𝐞𝐝 𝐠𝐥𝐚𝐫𝐞, 𝐰𝐡𝐞𝐫𝐞 𝐬𝐤𝐢𝐧 𝐦𝐞𝐞𝐭𝐬 𝐭𝐡𝐞 𝐞𝐱𝐭𝐫𝐞𝐦𝐞𝐬 𝐨𝐟 𝐬𝐧𝐨𝐰 𝐚𝐧𝐝 𝐬𝐮𝐧.

Cold & Heat Defense – Dynamic Barrier Protection – High-tech ExtrActive and phyto complex

INCI name

Glycerin, Aqua, Hippophae rhamnoides fruit extract

 

 
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Sea buckthorn berries, source of CRYOCARE® biomimetic active for cold and climate stress skin protection

Chitinase-powered skincare to face cold, heat & thermal shock

CRYOCARE® is a high-tech biomimetic active inspired by the adaptive strategies of Hippophae rhamnoides (sea buckthorn), a plant naturally exposed to severe climatic oscillations. Beyond its richness in omega fatty acids and antioxidant compounds, the fruit expresses chitinase, an adaptive ice-binding enzyme that supports cellular survival under freezing conditions.

Translating this biological strategy into skincare, CRYOCARE® targets the multi-layered impact of cold, heat and thermal shock, modulating the cellular processes that govern barrier stability, protein homeostasis and structural integrity.
Sudden temperature transitions — from freezing air to infrared heat — trigger vasoconstriction, dehydration, protein stress, mitochondrial ROS and lipid disorganization, progressively compromising barrier function.

By modulating these stress responses at their origin, CRYOCARE® helps the skin maintain functional balance during thermal challenges, reinforcing barrier properties, preserving structure and supporting comfort under extreme conditions of the modern exposome.

Thermal Stress & Skin Damage

  • Cold stress: significantly impacts skin tissue by inducing vasoconstriction and compromising the skin barrier, increasing dehydration, physical damage, and vulnerability to environmental aggressions. At the cellular level, it induces the formation of intracellular ice crystals, causing osmotic shock, membrane disruption, impaired enzymatic activity, and ultimately cell
    death.
  • Heat & infrared radiation: excessive heat and IR radiation induce ROS, denaturing proteins and oxidizing lipids, weakening the skin barrier and leads to dehydration, irritation, and accelerated aging. Thermal and IR exposure increase cellular burden, upregulating stress markers release and impairing mitochondrial function and reducing energy production while accelerating functional decline.
  • Thermal shock: rapid cold-to-heat shifts destabilize skin lipids and water balance, triggering micro-fissures and TEWL. Sudden transitions overactivate stress proteins and oxidative pathways, impairing cellular structure.

By activating biomimetic defense pathways, CRYOCARE® helps the skin maintain balance and resilience, offering effective protection against the diverse thermal challenges of the exposome.

EFFICACY TEST

Cold Shock Cell Survival

Rationale
Freezing exposure induces osmotic stress, intracellular ice formation and membrane damage, compromising keratinocyte viability.

Model
Cell viability has been assessed on Keratinocyte cell line exposed to hypothermic shock (two repeated exposures of 1 hour at -20°C) with or without CRYOCARE®.

Outcome
Cell viability significantly improved vs stressed control, confirming enhanced cold-shock tolerance.

Meaning
CRYOCARE® supports cellular integrity under acute cold exposure.

Graph showing improved keratinocyte viability after cold-shock exposure with CRYOCARE® compared to stressed control.

C-: cells not treated or exposed to thermal shock
C+: cells exposed to thermal shock

Hydration Maintenance Under Cold Stress (In Vivo)

Rationale
Low temperatures reduce lipid fluidity and disrupt the barrier, increasing TEWL and decreasing hydration.

Study
After baseline assessment, skin treated with CRYOCARE® (5%) or placebo was exposed to controlled cold and dry conditions (12 ± 2 °C; 35 ± 5% RH). Hydration was measured by Corneometer®.

Outcome
Improved hydration values vs placebo, demonstrating protection of water balance under cold stress.

Meaning
CRYOCARE® helps preserve skin comfort and hydration in cold conditions.

Skin hydration under cold exposure: CRYOCARE maintains moisture levels vs stressed control.

HEAT & IR-Induced Protein Stress Modulation (HSP72)

Rationale
Infrared radiation and thermal load elevate HSP72, a key marker of protein unfolding stress and mitochondrial ROS.

Model
Human keratinocytes subjected to photo-thermal stress (environmental temperature above 42°C and a total exposure of 300 J/m2 energy). CRYOCARE® applied at multiple concentrations; HSP72 quantified.

Outcome
Strong reduction of HSP72 overexpression vs stressed control.

Meaning
CRYOCARE® mitigates photothermal protein stress and supports cellular homeostasis.

IR-induced protein-stress modulation: reduction of HSP72 overexpression in keratinocytes treated with CRYOCARE.

THERMAL SHOCK MULTI-ENDPOINT STUDY

The experimental setup mimics real-life transitions—from freezing environments to heated spaces, and from hot, humid conditions to air-conditioned, cold-dry air—exposing skin to abrupt thermal and humidity shifts.

In a 3D full-thickness human skin model, 1.25 and 2.5 % CRYOCARE® were applied for 24 h before a thermal shock (–20 °C for 1 h, then +42 °C for 1 h).

a) Barrier Integrity (TEER)

Rationale
Rapid temperature shifts impair tight junctions and barrier resistance.

Model
Reconstructed epidermis exposed to cold-to-heat shock; TEER measured.

Outcome
Untreated epithelium lost ~60% TEER indicating tight junction disruption. CRYOCARE® showed TEER preservation vs stressed control.

Meaning
CRYOCARE® helps maintain barrier integrity during abrupt thermal transitions.

Barrier integrity under thermal-shock stress: TEER preservation after cold-to-heat transition with CRYOCARE.

b) Epidermal Structure

Rationale
Thermal shock induces micro-fissures and structural disorganization.

Model
Histological analysis post cold-to-heat stress.

Outcome
In the control (no stress) sample, the epidermis appears compact and continuous, with well-preserved nuclei (purple dots).

After cold-to-heat stress, the untreated skin shows clear damage: stratum corneum surface thinning; large vacuoles disrupting tissue structure; loss of nuclei indicating necrosis.

With CRYOCARE®, the epidermis retains a near-normal architecture: epidermal layer resembling control; vacuoles are reduced; nuclei remain visible.

Meaning
CRYOCARE® limits structural damage linked to thermal fluctuations.

Histological evaluation of epidermis after thermal shock: CRYOCARE reduces micro-fissures and preserves structure.
Histology section showing normal epidermal structure in untreated skin.

CONTROL

Histology image showing epidermal degeneration, necrosis and erosion under severe thermal shock.

COLD-TO-HEAT STRESSED

Histology image showing tissue preservation in cold-to-heat stressed skin treated with CRYOCARE® 1.25%.

COLD-TO-HEAT STRESSED 1.25% CRYOCARE

Histology image showing improved epidermal integrity under thermal stress with CRYOCARE® 2.5%.

COLD-TO-HEAT STRESSED 2.5% CRYOCARE

c) Type I Collagen

 Rationale
Thermal shock increases ROS and accelerates matrix degradation.

Model
Collagen I quantification and immunofluorescence under cold-to-heat stress.

Outcome

In the control (no thermal stress sample, collagen (green fluorescence) is homogeneously produced, dense and continuous (white arrow).

After cold-to-heat stress, untreated skin showed reduced and discontinuous collagen production (red arrow).

With CRYOCARE® treatment, collagen organization resembles the non-stressed control (yellow arrows): fibers appear denser and more continuous; structural gaps are reduced.

Meaning
CRYOCARE® helps preserve matrix integrity under extreme conditions.

Bar graph showing the preservation of Type I collagen in thermally stressed skin treated with CRYOCARE® at 1.25% and 2.5%, compared to untreated controls.
Fluorescent microscopy image showing baseline collagen I distribution in untreated epidermis.

CONTROL

Fluorescent image showing reduced collagen I signal after cold-to-heat stress.

COLD-TO-HEAT STRESSED

Fluorescent microscopy showing improved collagen I preservation in stressed skin treated with CRYOCARE® 1.25%.

COLD-TO-HEAT STRESSED 1.25% CRYOCARE

Fluorescent image showing strong collagen I preservation at 2.5% CRYOCARE® under thermal stress.

COLD-TO-HEAT STRESSED 2.5% CRYOCARE

Together, these results outline a robust, mechanism-supported efficacy profile for CRYOCARE®, validated across cellular, barrier, structural and matrix endpoints under extreme thermal stress.
  • Cold- and Heat-Stress Protection
    Helps modulate cellular responses activated by freezing temperatures and thermal load.
  • IR-Induced Protein-Stress Modulation
    Reduces heat-shock marker overexpression under infrared-driven protein unfolding.
  • Barrier Integrity Support Under Thermal Shock
    Contributes to maintaining tight-junction resistance and barrier continuity during abrupt temperature transitions.
  • Structural Preservation (Histology & Collagen I)
    Supports epidermal organization and matrix stability under extreme cold-to-heat fluctuations.
  • Hydration Maintenance in Cold Exposure
    Helps counter barrier impairment and dehydration caused by low-temperature environments.
  • Chitinase-Powered Biomimetic Strategy
    Inspired by ice-binding enzyme activity enabling survival in extreme climates.
  • High-Tech Extractive Process
    Refined fraction obtained through the Extractives technology for concentrated, reproducible performance.
  • Safe, Biodegradable & Regulation-Friendly
    Naturally derived active compliant with modern safety and sustainability standards.

ORIGIN

Plant extraction

 
   Appearance Clear Liquid
   Colour Light amber
   Odour Characteristic
   pH 4 – 6
   Dry residue (105°C) >90%
   Specific Gravity (25°C) 1.2 – 1.3

Ideal for emulsions and transparent water-based formulations, CRYOCARE® is recommended for:

  • Protective skincare in cold climates
  • Thermal care to prevent cold–heat shock damage
  • Urban skincare against exposoma stress
  • Sun care for reinforced climate defense
  • Well-aging solutions supporting collagen and elasticity
  • Repairing treatments for stressed and sensitive skin

% OF USE: 2.0 – 5.0%

 

 

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