For decades, anti-ageing skincare has primarily focused on correcting visible signs of ageing such as wrinkles, sagging, and uneven skin tones. However, as scientific understanding of ageing continues to evolve, the beauty industry is shifting toward a new paradigm: skin longevity.

Rather than simply targeting surface-level imperfections, longevity-oriented skincare aims to preserve the skin’s biological functionality over time. This emerging approach focuses on maintaining skin resilience, repair capacity, structural integrity, and overall cellular performance throughout the ageing process.

In this new era of longevity skincare, peptides and other advanced actives are evolving beyond traditional anti-ageing ingredients. As biological signaling molecules, peptide technologies are increasingly recognized for their ability to support multiple pathways associated with healthy skin ageing.

To better understand how Corum’s longevity science can contribute to skin longevity, we introduce the L.O.N.G.E.V.I.T.Y. Strategy — a multi-dimensional approach designed to support long-term skin functionality and resilience.

L — Long-Term Regenerative Capacity: Supporting Skin Functionality Against Stem Cell Exhaustion

One of the defining characteristics of youthful skin is its regenerative capacity, the ability to continuously renew, repair, and restore tissue functionality over time. Ageing-associated stem cell exhaustion is linked to reduced tissue renewal under steady-state conditions and impaired tissue repair following injury. In highly regenerative tissues such as the skin, maintaining cellular plasticity and repair-associated functions become increasingly important for preserving tissue functionality during ageing.¹

However, as ageing progresses, regenerative efficiency gradually declines due to stem cell exhaustion and reduced cellular adaptability. This loss of regenerative potential contributes to slower recovery, impaired repair responses, and visible signs of skin ageing.

Supporting long-term regenerative capacity therefore becomes a fundamental strategy in longevity-oriented skincare. Elastyl^TM MB/CC-MB helps support repair-associated cellular functions involved in skin regeneration and recovery.

• Elastyl^TM MB/CC-MB can stimulate fibroblast proliferation up to 150% at 20 ppm.
• Elastyl^TM MB/CC-MB can enhance fibroblast migration associated with wound healing activity up to 170.2% at 20 ppm.

By supporting regenerative functionality and adaptive recovery, peptide technologies may help maintain healthier skin performance throughout the ageing process.

O — Ongoing Stress Defense: Defending Against Stress-Induced Cellular Senescence

Throughout daily life, our skin is continuously exposed to environmental and biological stressors, including UV radiation, pollution, oxidative stress, and psychological burden, which can progressively compromise skin functionality over time. Beyond extrinsic aggressors, chronic stress has increasingly been recognized as a major contributor to stress-induced cellular senescence and premature skin ageing. Persistent stress can trigger biological processes associated with senescence, including impaired tissue repair, extracellular matrix deterioration, barrier dysfunction, and reduced adaptive capacity, ultimately contributing to functional decline during ageing.¹

Elevated cortisol levels induced by continuous stress exposure may impair skin barrier functionality, reduce adaptive recovery capacity, and accelerate stress-associated functional decline and cellular dysfunction over time.² Supporting the skin’s defense against ongoing stress therefore becomes an essential strategy in longevity-oriented skincare.

At the structural level, chronic stress can cause cellular senescence resulting in impaired collagen synthesis, accelerated ECM deterioration and visible skin ageing.^3,4 Corum’s Quintup^TM MB/CC-MB helps support ECM recovery under stress conditions by restoring collagen production following stress-induced damage.

• Quintup^TM MB/CC-MB can significantly restore collagen protein level production by 77% after cortisol damage.
• Quintup^TM MB/CC-MB can also restore collagen protein level production by 46% after UVA damage.

In addition to ECM alteration, cortisol may also repress Calpain-1 activity, potentially disrupting filaggrin processing and reducing natural moisturizing factor (NMF) production, ultimately contributing to dry and senescence-associated skin dysfunction.

• Elastyl^TM MB/ CC-MB can restore Calpain 1(CAPN1) activity up to 94.24% after cortisol damage, enhancing filaggrin processing and promoting NMFs on stressed and tired skin.

By supporting stress recovery pathways and adaptive resilience, Quintup^TM MB/CC-MB and Elastyl^TM MB/CC-MB may help reduce stress-associated functional decline during skin ageing.

N — Nucleus Stability: Protecting Skin Against Genomic Instability

The nucleus serves as the control center of the cell, housing genetic information essential for cellular function, repair, and regeneration. However, cumulative environmental stress can contribute to genomic instability and DNA damage, gradually impairing cellular functionality and adaptive resilience over time.¹ Maintaining genomic integrity is therefore becoming an increasingly important aspect of longevity-oriented skincare.

Nutecyl^TM MB/CC-MB helps protect genomic integrity by reducing environmentally induced DNA damage and supporting healthier cellular functionality.

• Nutecyl^TM MB/ CC-MB offers a 53% protection rate against H2O2-induced DNA damage at 40 ppm.
• Nutecyl^TM MB/ CC-MB significantly reduced UVR-induced DNA damage in HaCaT cells by 96% at 10 ppm.

By helping preserve genomic integrity and reduce cumulative DNA damage, Nutecyl^TM MB/CC-MB may support long-term cellular performance and healthier skin ageing.

G — Guardian of Proteostasis: Protecting Skin Against Loss of Proteostasis

Proteostasis, the maintenance of properly functioning proteins within cells, is essential for healthy skin ageing. As skin ages, damaged, misfolded, or glycated proteins gradually accumulate, impairing protein quality control systems and disrupting cellular homeostasis. This progressive loss of proteostasis is increasingly recognized as one of the major hallmarks contributing to functional decline associated with ageing.¹

Among the factors contributing to proteostasis loss, glycation and impaired protein quality control play complementary roles. Glycation occurs when excess sugars non-enzymatically react with structural proteins such as collagen and elastin, leading to the formation of advanced glycation end products (AGEs). The accumulation of AGEs impairs protein functionality, reduces structural flexibility, and accelerates the deterioration of skin structure during ageing.¹

Meanwhile, Heat Shock Protein 47 (HSP47) is a collagen-specific molecular chaperone that plays a critical role in collagen folding, maturation, and quality control. By supporting collagen homeostasis, HSP47 contributes to maintaining extracellular matrix integrity and preserving protein functionality during ageing.⁸

To support multiple aspects of proteostasis, CORUM combines complementary longevity technologies targeting both protein protection and protein quality control.

Nutecyl^TM MB/CC-MB helps reduce glycation-associated protein damage by inhibiting AGE formation.

• Nutecyl^TM MB/CC-MB inhibits AGE-BSA formation by 30.8% at 10.8mM.

Tricoll^TM MB/CC-MB supports collagen quality control by enhancing HSP47 expression.

• Tricoll^TM MB/CC-MB increases HSP47 production by 81% at 5 ppm.

By reducing glycation-associated protein damage while supporting collagen quality control, Nutecyl^TM MB/CC-MB and Tricoll^TM MB/CC-MB help preserve protein homeostasis, contributing to healthier skin functionality and long-term resilience during ageing.

E — ECM Homeostasis: Addressing Altered Extracellular Matrix Properties During Ageing

The extracellular matrix (ECM) is far more than a structural scaffold. Increasingly, it is recognized as a dynamic microenvironment responsible for cellular communication, tissue organization, repair signaling, and mechanical resilience.⁵ During ageing, ECM fragmentation and collagen degradation progressively disrupt these biological networks, accelerating structural and functional decline within the skin.⁶ Maintaining ECM homeostasis therefore requires a coordinated strategy involving collagen synthesis, degradation control, elasticity preservation, and structural support.

Tricoll^TM MB/CC-MB, Defensyl^TM MB/CC-MB, Quintup^TM MB/CC-MB, and Elastyl^TM MB/CC-MB collectively support ECM-related longevity pathways associated with healthier skin structure and resilience.

Tricoll^TM MB/CC-MB helps support collagen preservation and ECM integrity by reducing collagen degradation and promoting collagen synthesis.

• Tricoll^TM MB/CC-MB down-regulates MMP-1 expression by 55% at 10 ppm following UVA exposure.
• Tricoll^TM MB/CC-MB stimulates protein-level collagen synthesis by 57% at 10 ppm.

Defensyl^TM MB/CC-MB helps protect ECM functionality under blue light-induced stress conditions by supporting collagen preservation pathways.

• Defensyl^TM MB/CC-MB down-regulates MMP-1 expression by 38% at 10 ppm following blue light exposure.
• Defensyl^TM MB/CC-MB restores collagen levels by 15% following blue light exposure at 10 ppm.

Quintup^TM MB/CC-MB supports collagen-related pathways associated with ECM maintenance and structural longevity.

• Quintup^TM MB/CC-MB up-regulates ECM-related mRNA expression, including COL1A1 (+92%), COL4A1 (+74%), FN-1 (+30%), and TGFB-1 (+22%) at 10 ppm.
• Quintup^TM MB/CC-MB stimulates collagen type I protein expression by 51% at 5 ppm.

Meanwhile, Elastyl^TM MB/CC-MB contributes to elastin-related pathways associated with skin elasticity and structural adaptability.

• Elastyl^TM MB/CC-MB stimulates natural elastin synthesis by 167% at 40 ppm
• Elastyl^TM MB/CC-MB stimulates elastin protein production by 421% at 10 ppm on healthy skin.
• Elastyl^TM MB/CC-MB restores elastin protein production by 121% at 10 ppm on UVB-damaged skin.

Together, these peptides help support ECM homeostasis associated with long-term skin resilience and structural longevity.

As ECM integrity plays a central role in skin structure, elasticity, and tissue recovery, improvements at the molecular level may ultimately translate into visible skin benefits. While longevity science often focuses on biological mechanisms, visible skin recovery remains one of the most meaningful indicators of skin functionality and resilience. As skin ages, its ability to recover from environmental stress gradually declines, leading to prolonged roughness, reduced elasticity, and visible skin fatigue. Supporting visible recovery therefore becomes an important component of longevity-oriented skincare.

Tricoll^TM MB/CC-MB, Defensyl^TM MB/CC-MB, Quintup^TM MB/CC-MB, and Elastyl^TM MB/CC-MB help support skin recovery pathways associated with healthier and more resilient skin appearance. In vivo studies demonstrated improvements in skin smoothness, wrinkle appearance, and structural skin recovery.

• 3% Tricoll^TM MB/CC-MB and 1% Defensyl^TM MB/CC-MB improved crow's feet appearance, with reduced skin roughness observed in 60% of volunteers after 28 days of application. An average reduction of 4% was observed across all subjects
• 5% Quintup^TM MB/CC-MB reduced neck wrinkles by 51.32% and barcode wrinkles by 30.58% after 56 days of application, while increasing collagen content by 7.1% compared to the placebo group.
• 5.5% Elastyl^TM MB/CC-MB improved skin firmness in 90% of volunteers after 28 days of application, increasing suppleness by 57.6% and firmness by 51.1%.
• 5% Elastyl™ MB/CC-MB reduced the appearance of lip lines after 5 days of application.

By supporting ECM properties, visible recovery responses, and improving skin quality, these peptides may help maintain healthier-looking skin throughout the ageing process.

V — Vitality Preservation: Addressing Epigenetic Alteration During Ageing

Ageing is not only driven by structural decline, but also by progressive alterations in cellular programming. Over time, accumulated environmental stress and biological damage can disrupt youthful gene expression patterns, alter epigenetic regulation, and abnormal post-translational modification of histones. These epigenetic alterations are increasingly recognized as important contributors to functional and visible skin ageing.¹

Supporting the preservation of youthful cellular functionality therefore becomes an important strategy in longevity-oriented skincare. Epi-On® helps support epigenetic pathways associated with healthier and more resilient skin ageing through HDAC inhibition and enhanced histone acetylation, two mechanisms closely associated with epigenetic regulation and cellular functionality.¹

• Epi-On® inhibits HDAC activity by 63.2% at 0.5%.
• Epi-On® increases histone acetylation (H4K16ac) expression by 269% in keratinocytes and 246% in fibroblasts at 0.5%.

Next-generation sequencing (NGS) analysis further demonstrated that Epi-On® regulates genes associated with growth factors, cellular vitality, and inflammatory responses, supporting healthier cellular functionality and adaptive resilience. Beyond epigenetic regulation, Epi-On® also supports cellular functions associated with tissue renewal and regeneration. Improved cellular migration and structural integrity may help maintain healthier skin functionality throughout the ageing process.

• At 0.05%, Epi-On® promotes keratinocyte migration by 153.9% and fibroblast migration by 84.8%.
• At 4%, Epi-On® increases fibronectin protein expression by 59% at the edge of lesions in the papillary dermis in an ex vivo study.
• At 4%, Epi-On® increases Integrin β4 expression by 14% at the dermal-epidermal junction (DEJ) edge in an ex vivo study.

These improvements in cellular functionality, tissue renewal, and structural integrity may ultimately translate into visible skin recovery benefits.

Clinical studies further demonstrated accelerated skin recovery benefits of Epi-On® following laser treatment. Immediate reductions in erythema and skin redness were observed after treatment, with continued improvement over time. After 5 days, erythema color was reduced by up to 60%, demonstrating enhanced skin recovery and resilience.

By helping preserve youthful cellular programming, maintain epigenetic functionality, and support skin structure integrity, Epi-On® contributes to a more longevity-oriented approach to resilient skin ageing.

I — Inflammageing Control: Targeting Chronic Inflammation Associated with Skin Ageing

Chronic low-grade inflammation, commonly known as inflammageing, is increasingly recognized as a key contributor to accelerated biological ageing.^1,7 Environmental stressors such as UV radiation and blue light exposure can trigger pro-inflammatory cascades, progressively impairing skin functionality and accelerating ECM degradation over time.¹ Controlling chronic inflammation therefore becomes an essential strategy in longevity-oriented skincare.

Defensyl^TM MB/CC-MB helps support healthier skin ageing by modulating inflammation-related pathways associated with environmental stress exposure.

• At 10ppm, Defensyl^TM MB /CC-MB significantly reduces multiple pro-inflammatory mediators associated with UV- and blue light-induced skin stress, including:
  • Reduction of UVB-induced IL-6 by 37%
  • Reduction of blue light-induced IL-6 by 40%
  • Reduction of blue light-induced IL-8 by 14%
  • Reduction of blue light-induced COX-2 by 28%

By helping regulate chronic inflammation and reduce environmental stress-induced inflammatory responses, Defensyl^TM MB/CC-MB may support healthier, more resilient skin.

T — Thriving Bioenergetics: Counteracting Mitochondrial Dysfunction During Ageing

Mitochondria are the primary energy-producing organelles that regulate cellular bioenergetics, redox homeostasis, and adaptive stress responses. During ageing, mitochondrial dysfunction progressively compromises mitochondrial quality and cellular metabolism, contributing to functional decline across multiple hallmarks of ageing.¹

Maintaining mitochondrial function has therefore emerged as an important strategy in longevity-oriented skincare. Beyond cellular energy production, healthy mitochondria also help maintain redox homeostasis and adaptive cellular resilience. Revityl^TM supports mitochondrial function through complementary mechanisms involving mitochondrial biogenesis, antioxidant defense, and cellular bioenergetics.

1. Supporting Mitochondrial Biogenesis:

Healthy mitochondrial function depends on efficient mitochondrial biogenesis and respiratory capacity. Revityl^TM supports mitochondrial biogenesis and energy metabolism by upregulating genes associated with mitochondrial function.

• Revityl^TM restores NRF1 gene expression by 56% at 10 ppm, supporting mitochondrial biogenesis.
• Revityl^TM upregulates mitochondrial-related genes involved in mitochondrial function, including:
  • MT-ND6 by 39% at 10 ppm
  • SDHB by 28% at 5 ppm

2. Strengthening Mitochondrial Antioxidant Defense:

Mitochondria are a major source of reactive oxygen species (ROS). During ageing, excessive mitochondrial oxidative stress accelerates mitochondrial dysfunction and contributes to cellular damage.¹ Revityl^TM helps maintain mitochondrial redox homeostasis by enhancing endogenous antioxidant defense.

• Revityl^TM increases SOD2 gene expression by 30% at 10 ppm after UVB exposure.
• Revityl^TM significantly reduces mitochondrial superoxide production by 58.2% at 10 ppm after oxidative stress damage.

3. Enhancing Mitochondrial Function:

Improved mitochondrial membrane potential and oxidative balance ultimately translate into healthier mitochondrial function. Revityl^TM helps preserve mitochondrial activity while reducing oxidative DNA damage.

• Revityl^TM enhances overall mitochondrial membrane potential (mitochondrial activity) by 49.3% at 5 ppm after oxidative stress damage.
• Revityl^TM reduces DNA damage by 32% at 5 ppm after oxidative stress damage.

By supporting mitochondrial biogenesis, strengthening antioxidant defense, and improving mitochondrial performance, Revityl^TM helps maintain cellular bioenergetics, adaptive resilience, and healthier skin functionality during ageing.

Y — Youthful Communication: Addressing Altered Intercellular Communication During Ageing

One of the important aspects of skin ageing is the progressive disruption of intercellular communication.¹ As skin ages, environmental stress and accumulated cellular damage can alter the production of signaling molecules that coordinate communication between keratinocytes, fibroblasts, and melanocytes. This dysregulated communication may contribute to uneven skin tone, age-associated pigmentation, and other visible signs of skin ageing. Among these communication pathways, pigmentation-related signaling plays a particularly important role in age-associated skin appearance.⁹

Age-associated pigmentation, including uneven skin tone and age spots, is increasingly recognized as a consequence of altered communication between keratinocytes, fibroblasts, and melanocytes.⁹ Under environmental stress conditions, signaling molecules such as Endothelin-1 (ET-1), α-MSH, and Stem Cell Factor (SCF) may become overexpressed, continuously stimulating melanocytes and contributing to persistent hyperpigmentation.

GenoWhite® helps support healthier skin communication by regulating upstream pigmentation-related signaling pathways associated with ageing and environmental stress.

• GenoWhite® downregulates ET-1 secretion by 92.7% at 0.4% after UVB irradiation.
• GenoWhite® inhibits α-MSH-induced tyrosinase activity by 40% at 0.3%.
• GenoWhite® downregulates SCF secretion by 61.3% at 0.2% following UVB irradiation.

Clinical studies further demonstrate the visible benefits of regulating pigmentation-related communication pathways during ageing.

• GenoWhite® reduces age spot appearance by 87.4% with a 2% cream after 56 days of application.

By helping regulate pigmentation-related communication pathways associated with ageing and environmental stress, GenoWhite® contributes to a more longevity-oriented approach to skin radiance, tone uniformity, and healthier pigmentation balance. In this evolving perspective, youthful skin is not simply skin that looks younger — it is skin that continues to communicate, adapt, and maintain biological balance over time.

A New Paradigm for Resilient Ageing

The shift from traditional anti-ageing toward Skin Longevity represents a fundamental evolution in skincare science. Rather than focusing solely on correcting visible signs of ageing, longevity-oriented skincare aims to preserve the biological functionality, adaptability, and communication networks that support healthy skin over time.

As the hallmarks of ageing become increasingly interconnected, maintaining youthful skin can no longer rely on single target approaches alone. Instead, healthier skin ageing requires a multidimensional strategy capable of supporting regeneration, stress adaptation, proteostasis, genomic integrity, ECM integrity, inflammageing balance, epigenetic functionality, mitochondrial functionality, and intercellular communication simultaneously.

Through Corum’s L.O.N.G.E.V.I.T.Y. Strategy, these longevity-oriented actives are strategically applied to support multiple biological pathways associated with long-term skin functionality and adaptability. Ultimately, skin longevity is not only defined by the absence of wrinkles, but also by the skin’s ability to continuously communicate, recover, adapt, and maintain functional integrity throughout the ageing process.

By targeting multiple hallmarks of ageing, Corum’s longevity strategy helps support skin that remains resilient, responsive, and radiant far beyond the surface. Because longevity is not about stopping skin ageing, it is about helping skin remain resilient enough to age beautifully.

References

1. López-Otín, C., Blasco, M. A., Partridge, L., Serrano, M., & Kroemer, G. (2023). Hallmarks of aging: An expanding universe. Cell, 186(2), 243–278. https://doi.org/10.1016/j.cell.2022.11.001
2. Altemus, M., Rao, B., Dhabhar, F. S., Ding, W., & Granstein, R. D. (2001). Stress-induced changes in skin barrier function in healthy women. The Journal of investigative dermatology, 117(2), 309–317. https://doi.org/10.1046/j.1523-1747.2001.01373.x
3. Qin, T., Chen, T., Ma, R., Li, H., Li, C., Zhao, J., Yuan, J., Zhang, Z., & Ning, X. (2024). Stress Hormones: Unveiling the Role in Accelerated Cellular Senescence. Aging and disease, 16(4), 1946–1970. https://doi.org/10.14336/AD.2024.0262
4. Domaszewska-Szostek, A., Puzianowska-Kuźnicka, M., & Kuryłowicz, A. (2021). Flavonoids in Skin Senescence Prevention and Treatment. International journal of molecular sciences, 22(13), 6814. https://doi.org/10.3390/ijms22136814
5. Theocharis, A. D., Skandalis, S. S., Gialeli, C., & Karamanos, N. K. (2016). Extracellular matrix structure. Advanced drug delivery reviews, 97, 4–27. https://doi.org/10.1016/j.addr.2015.11.001
6. Quan, T., & Fisher, G. J. (2015). Role of Age-Associated Alterations of the Dermal Extracellular Matrix Microenvironment in Human Skin Aging: A Mini-Review. Gerontology, 61(5), 427–434. https://doi.org/10.1159/000371708
7. Franceschi, C., Garagnani, P., Parini, P., Giuliani, C., & Santoro, A. (2018). Inflammaging: a new immune-metabolic viewpoint for age-related diseases. Nature reviews. Endocrinology, 14(10), 576–590. https://doi.org/10.1038/s41574-018-0059-4
8. Ito, S., & Nagata, K. (2017). Biology of Hsp47 (Serpin H1), a collagen-specific molecular chaperone. Seminars in cell & developmental biology, 62, 142–151. https://doi.org/10.1016/j.semcdb.2016.11.005
9. Imokawa G. (2004). Autocrine and paracrine regulation of melanocytes in human skin and in pigmentary disorders. Pigment cell research, 17(2), 96–110. https://doi.org/10.1111/j.1600-0749.2003.00126.x