The Company

Leading the quest for drugs against aging

Everon Biosciences, Inc. was founded in 2010 with the goal of developing anti-aging medicines. Company’s scientific program and vision are based on principles of eradicating the cellular foundations of aging formulated by Prof. Andrei Gudkov, Senior Vice President of Research Programming and Development of Roswell Park Cancer Institute, the world’s oldest cancer research center. From the very beginning, the institute has been Everon’s supportive shareholder and a reliable partner, providing access to its rich technical infrastructure and its scientists and physicians. This strategic collaboration resulted in the development of pharmacological and immunological approaches to treatment of age-related frailty. Everon holds a unique position among recently launched anti-aging companies in its approach to the treatment of aging from all major R&D aspects: mechanistic understanding of aging process, access to targets, availability of proprietary drug candidates, strong preclinical efficacy indications, the development of diagnostic tools and clinical strategy.

Our Approach

Anti-aging therapeutics have long been a topic for fiction writers rather than pharmacologists. The situation has radically changed today, with aging treatment turning into a more and more realistic opportunity being explored by several recently launched companies ( read our white paper CONFRONTING THE LAW OF NATURE ). Everon’s approach is unique and comprehensive. Its major conceptual and technological cornerstones are summarized below:

  • Aging is a physiologically programmed process that is pre-determined at the DNA level. Because of that, the onset of systemic physiological decline (frailty) occurs at a genetically defined age that varies across mammalian species.
  • The accumulation of aging-associated frailty can occur independently of the acquisition of age-related diseases; however, the risk of the latter is increased in a frail organism and can accelerate aging.
  • Molecular genetic mechanism identified by Everon researchers in partnership with Roswell Park Cancer Institute scientists serves as a program underlying aging. This mechanism explains the gradual accumulation of cellular and extracellular waste products that poison the microenvironment of aging tissues.
  • The gradual accumulation of waste products with age exhausts the “waste removal” branches of the immune system; this in turn leads to its malfunction and to the development of sterile chronic inflammation.
  • Aging can be quantitatively measured. Everon has implemented three robust diagnostic tools for detecting changes in physiological age; these tools are essential for assessing the efficacy of anti-aging drugs:
  • Frailty Index (FI) as a measure of age-related malfunction of all body components;
  • A proprietary bioinformatics tool for the detection of aging biomarkers in DNA samples from somatic cells of human and mouse;
  • An optical device combined with subcutaneous diagnostic assay for the functional assessment of objective biological age.
Based on the above, Everon has launched an R&D program aimed at (i) developing pharmacological agents (small molecules and immunotherapeutics) that can block or slow down the generation of age-related waste products, (ii) restoring or facilitating the efficacy of natural mechanisms removing accumulated waste and (iii) creating a diagnostic platform to accurately estimate the severity of aging-related frailty and efficacy of antiaging drugs.
Recently, Everon scientists discovered and patented a new cellular target likely to be the dominant root cause of systemic poisoning and inflammation. This sets the company apart from its main competitors who only pursue senolytics (agents eliminating senescent cells) as potential anti-aging drugs.
Currently, Everon is optimizing several lead compounds: small molecules and biologics that have already demonstrated a rejuvenation effect in aging animals, as measured by a lowered mouse FI (similar FI has recently been accepted by FDA as a measure of aging in the ongoing Metformin human trial). In preliminary experiments, rejuvenated animals live on average 25-30% longer, and this number is expected to increase as optimization continues.
Understanding the molecular genetic mechanisms underlying aging has put the Everon-RPCI alliance into a unique position, enabling them, for the first time, to target the basic foundation of the endogenous aging program and to extend their R&D efforts – from treating or preventing aging-associated health decline – to the treatment and prevention of the aging program itself.

The Team

Alexander Polinsky Ph.D.
Alexander Polinsky Ph.D. Founder
Chief Executive Officer
Andrei Gudkov Ph.D., DSci
Andrei Gudkov Ph.D., DSci Founder
Chief Scientific Officer
Olga Chernova Ph.D.
Olga Chernova Ph.D. Founder
VP Research
Aleksandra Kotlyarova
Aleksandra Kotlyarova Director of Operations
Brandon Hall Ph.D.
Brandon Hall Ph.D. Small Molecules, Cell Biology
David Frescas Ph.D.
David Frescas Ph.D.Immunology
Anatoli Gleiberman Ph.D.
Anatoli Gleiberman Ph.D. Histology
Pavel Komarov Ph.D.
Pavel Komarov Ph.D. High-Throughput Screening
Ekaterina Andrianova Ph.D.
Ekaterina Andrianova Ph.D. Development
Denis Kazulkin Ph.D.
Denis Kazulkin Ph.D. Medicinal Chemistry
Vitaly Balan Ph.D.
Vitaly Balan Ph.D. Polymer Beads, Liposomes
Peter Krasnov Ph.D.
Peter Krasnov Ph.D. Cell Biology
Marina Antoch, Ph.D.
Marina Antoch, Ph.D. Animal Experiments



David Frescas et al (2017) Murine mesenchymal cells that express elevated levels of the CDK inhibitor p16(Ink4a) in vivo are not necessarily senescent (

Brandon Hall et al (2017) p16(Ink4a) and senescence-associated β-galactosidase can be induced in macrophages as part of a reversible response to physiological stimuli ( or (

M. Antoch et al (2017) Physiological frailty index (PFI): quantitative in-life estimate of individual biological age in mice (

D. Frescas et al (2017) Senescent cells expose and secrete an oxidized form of membrane-bound vimentin as revealed by a natural polyreactive antibody (

B. Hall et al (2016) Aging of mice is associated with p16(Ink4a)- and β-galactosidase-positive macrophage accumulation that can be induced in young mice by senescent cells (


The Biology of Aging: Advances in Therapeutic Approaches to Extend Healthspan; SCRIPPS, Jupiter, FL, January 22-25, 2017

  • A. Gudkov’s Lecture: Small molecule that extends life- and health-span in a mouse model of chronological aging: molecular mechanisms and cellular targets (VIDEO)
  • B. Hall et al (POSTER) p16(Ink4a) and Senescence-Associated β-galactosidase (SABG) as Markers of Reversible Physiological Response in Macrophages
  • D. Frescas et al (POSTER) Senescent cells expose and secrete a novel oxidized form of membrane-bound vimentin as revealed by a natural polyreactive antibody
  • M. Antoch et al (POSTER) Defining biological age of individual mice by creating the Frailty Index
  • E. Leonova et al (POSTER) Systemic DNA damage stays indefinitely dormant or turns into accelerated aging depending on life conditions
  • I. Gitlin et al (POSTER) Is inflammaging essential for mouse aging?

Cellular Senescence: From Molecular Mechanisms to Therapeutic Opportunities; Weizmann Institute, Rehovot, Israel, July 3-6, 2016

  • A.Gudkov’s Lecture: Biological sense of senescent cells (VIDEO)

Andrei Gudkov`s TEDx talk on May 28, 2017: Can we stop aging? (VIDEO)

Contact Us


Everon Biosciences, Inc.
640 Ellicott St., Suite 444
Buffalo, NY 14203
Phone: 716.858.3055
Fax: 716.858.3044