The 2025 Nobel Prize in Physiology or Medicine was awarded to the crucial "braking mechanism" in the immune system - regulatory T cells (Treg), which can suppress chronic inflammatory states, target the elimination of senescent cells, and strengthen the dialogue between the skin barrier and the immune system. And PDRN seems to have something in common with this mechanism.

What is PDRN?

PDRN (polydeoxyribonucleotides) is a highly purified polymer of DNA fragments known for its excellent safety and stability. It is primarily derived from salmon sperm. While PDRN has been used in clinical practice for long time, its application in cosmetics is relatively new. It typically appears under registered names such as Sodium DNA or Deoxyribonucleic Acid.

Effects of PDRN

ü  Promotes collagen synthesis

ü  Improves skin elasticity and reduces wrinkles

ü  Accelerates wound healing

ü  Anti-inflammatory; supports acne scar treatment

ü  Reduces melanin production

ü  Promotes hair regeneration, increases hair thickness, and supports hair follicle growth

The mechanism of action of PDRN

Activation of the Adenosine A2A Receptor:

PDRN is cleaved into adenosine monomers under the action of nucleases, which then bind to and activate the adenosine A2A receptor, triggering a cascade of downstream responses. This activation upregulates IL-10 (an anti-inflammatory cytokine), VEGF, and other growth factors, while downregulating inflammatory cytokines such as TNF-α, IL-6, and IL-8. As a result, it promotes collagen and fibrin production and ultimately delivers anti-inflammatory effects, stimulates collagen synthesis, and accelerates wound healing.

(By promoting VEGF expression, newly formed capillaries supply nutrients for skin repair and help remove metabolic waste. Meanwhile, enhanced proliferation of fibroblasts and increased secretion of EGF, FGF, and IGF contribute to restoring the skin’s damaged microenvironment.)

Salvage Pathway:

The purine and pyrimidine bases generated from PDRN degradation are utilized by cells for DNA repair and nucleotide synthesis, thereby supporting cellular growth and enhancing cell viability.

Other Mechanisms of Action:

Downregulation of MITF:

MITF is a transcription factor that activates genes responsible for melanin production, including tyrosinase, TRP-1, and TRP-2 (all of which promote melanogenesis). PDRN reduces the levels of MITF, thereby inhibiting melanin synthesis.

Activation of Hair Follicle Regeneration Pathways:

PDRN stimulates growth factors associated with hair follicle regeneration, leading to thickening of existing hair shafts and overall improvement in follicle health.

PDRN Production Processes:

Traditional animal-derived extraction: DNA fragments are extracted from salmon testes or eggs.

Synthetic biology: Engineered microorganisms (such as E. coli or lactic acid bacteria) are used to express specific DNA fragments.

Plant-derived extraction and synthesis: Callus tissues are induced from plant leaves (e.g., Gynostemma pentaphyllum, rose). DNA fragments are then extracted using ultrasonic treatment, and plant genomic DNA is cut to the desired molecular weight using restriction endonucleases.

PDRN’s evolution—from its role in regenerative medicine in the 1980s to its integration into modern skincare formulations—demonstrates the power of science-backed innovation in cosmetic science.

With proper formulation and delivery, PDRN-based skincare can offer unparalleled benefits, boosting hydration, improving skin texture, and enhancing elasticity.

The global demand for PDRN skincare highlights one key point: consumers increasingly value scientifically validated, results-driven formulations. With its remarkable efficacy and rising popularity, PDRN is poised to reshape the anti-aging skincare landscape in the coming years.

References

Polydeoxyribonucleotide in Skincare and Cosmetics: Mechanisms, Therapeutic Applications, and Advancements Beyond Wound Healing and Anti-aging（2025）

Efficacy Study of PDRN Essence after Non-ablative Fractional Laser on Facial Rejuvenation（2025）

Graft Versus Host Disease: New Insights into A2A Receptor Agonist Therapy. (2015)