Rejuvenating extracellular matrix to fight aging
Our mission is to develop a therapy that prevents age-related degradation of the extracellular matrix (ECM). We are focused on small molecules that have the potential to slow down aging, and protect people from diabetes, cardiovascular and Alzheimer’s diseases, by inhibiting cross-linking in the extracellular matrix. Boston Matrix is ​​a nonprofit project. Our research and development process is transparent, and results are reported openly.
As we age, these proteins form chemical bonds with each other, called cross-links. This reduces the elasticity of the matrix, promoting inflammation and tissue degeneration. Our goal is to develop a drug that destroys the cross-links and/or inhibits their formation.
ECM and Aging
The extracellular matrix (ECM) fills the spaces between cells and serves as an internal network that connects the entire body. It makes up more than 30% of the body weight of an adult. Most of the ECM proteins (collagens and elastins) are formed during childhood and are poorly restored.
Blood sugar reacts with matrix proteins to form compounds called advanced glycation endproducts (AGEs).

The endproducts of glycation can subsequently react with other proteins to form difficult-to-break cross-links. Such cross-links play the role of molecular "handcuffs" that bind adjacent protein molecules and prevent them from moving independently. As a result, the matrix loses its elasticity and becomes more rigid.

For example, in the skin, such changes appear in the form of wrinkles and loss of elasticity. An increase in the rigidity of the matrix is ​​associated with the thickening of blood vessel walls, changes in the tissues of the heart, the development of a number of oncological, and neurodegenerative, and other age-related diseases.
Causes of ECM aging
Cellular senescence
Chronic inflammation
Decreased self-renewal ability of cells
Stem cells niches disruption
Aging
Decreased tissue elasticity
Neurodegeneration
Diseases of the cardiovascular system
Matrix aging dynamics
Crosslinks accumulation is the main source of collagen structure impairment. It leads to deterioration in the availability of collagens for enzymes involved in matrix renewal. As the result, regeneration of ECM becomes impossible.
Dynamic of scientific studies
According to the scientific database Scopus, over the last few years, there has been a significant increase in the number of scientific papers in the field of AGE and ECM aging.
AGE molecules/ ECM crosslink types
Here are the most dangerous and widespread AGEs: their characteristics, related diseases and precursors available for therapy.
Formula
(click to open the topic)
The product is the result of oxidative processes
Products from which it is formed
Properties
Precursors hypothetically available for pharmacological action
Glucosepane
Degradation of Amadori products or methylglyoxal + lysine and arginine residues.
Does not fluoresce, crosslinks.
Amadori product or methylglyoxal.
Associations with diseases
Formula
(click to open the topic)
The product is the result of oxidative processes
Products from which it is formed
Properties
Precursors hypothetically available for pharmacological action
Crossline
Degradation of Amadori products + two lysine residues.
Fluorescent (λexc = 379, λem = 463), crosslinks.
Amadori product.
Associations with diseases
Formula
(click to open the topic)
The product is the result of oxidative processes
Products from which it is formed
Properties
Precursors hypothetically available for pharmacological action
Nε-Carboxymethyllysine (CML)
3-deoxyglucosone or glyoxal + lysine residue.
Non-fluorescent, non-crosslinking.
Glyoxal, glycoaldehyde, 3-deoxyglucosone.
Associations with diseases
Formula
(click to open the topic)
The product is the result of oxidative processes
Products from which it is formed
Properties
Precursors hypothetically available for pharmacological action
MOLD
Yes (due to the role of oxidative processes in the formation of methylglyoxal).
Methylglyoxal + 2 lysine residues.
Does not fluoresce, crosslinks (more).
Methylglyoxal.
Associations with diseases
Cataracts (source 1, source 2)
Formula
(click to open the topic)
The product is the result of oxidative processes
Products from which it is formed
Properties
Precursors hypothetically available for pharmacological action
Pentosidine
Degradation of Amadori products + lysine and arginine residues.
Fluorescent (λexc = 335, λem = 385), crosslinks.
Amadori products.
Associations with diseases
Formula
(click to open the topic)
The product is the result of oxidative processes
Products from which it is formed
Properties
Precursors hypothetically available for pharmacological action
Nε-Carboxyethyllysine (CEL)
Methylglyoxal + lysine residue.
Non-fluorescent, non-crosslinking.
Methylglyoxal.
Associations with diseases
Formula
(click to open the topic)
The product is the result of oxidative processes
Products from which it is formed
Properties
Precursors hypothetically available for pharmacological action
Vesperlysine A, B
Degradation of Amadori products + two lysine residues.
Fluorescent (λexc = 366, λem = 442), crosslinks.
Glyoxal, glycoaldehyde, 3-deoxyglucosone, Amadori products.
Associations with diseases
Boston matrix is ​​an open source project dedicated to the combating of extracellular matrix aging. Collaboration with the international expert community is necessary to achieve the fastest possible result. Therefore, we invite scientific groups and other specialists from all over the world to participate in our endeavour. Join us If you share our philosophy and vision. Currently, BM develops two approaches: one of them is breaking crosslinks of matrix proteins, and the other is preventing the negative effects of crosslink formation. We strive for open collaboration with the global expert community to achieve the fastest results possible.
We are building a bioinformatic platform for screening molecules — "expanding" intermediate and endproducts of glycation (AGE), with subsequent validation in cell cultures and model animals.
In parallel, we are working on the screening and development of RAGE (receptor for advanced glycation endproducts) blocking molecules, through which AGEs induce inflammation and tissue degeneration.
About Our Project
The results of the project will form the basis for the development of a drug with a double protective effect: protecting blood circulation and metabolism in the nervous system.
Our solutions
Dynamics of progress in the development of our ECM protective and rejuvenating products.
clinical trials
in silico
analysis of candidate molecules
in vivo
pre-clinical
Anti AGEs
More →
RAGE-inhibitors
in vitro
chemical synthesis
model adaptation
screening
Anti AGEs: breaking crosslinks and adducts
Testing the molecules in cell cultures on a glycated collagen matrix
Bioinformatic screening of candidate molecules
Modeling the formation of crosslinks and adducts
Testing on model animals
Clinical trials
RAGE-inhibitors: receptor blockers
Testing the molecules in cell cultures in the presence of AGE
AGE-based pharmacological blocker design
In Silico modeling the interaction between AGE and RAGE
Testing on model animals
Clinical trials
Collaborations and Microgrants
Boston Matrix is an open-source project and we are interested in connecting with scientists of various specializations to jointly approach the problem of ECM cross-links. We also provide micro-grants for collaborative research to fight the aging of the ECM.
Team
Roman Litvinov, M.D., Ph.D.
Head of Research
Nikita Valuyskiy
Researcher
Marina Gasheva
Researcher
Timofey Glinin, Ph.D.
CSO, Open Longevity
Anastasia Egorova
CEO, Open Longevity
Konstantin Dremov
CBDO
Dora Bataeva
Biotech analyst, Representative in Toronto, Canada
Svetlana Bozrova, Ph.D.
Biologist, Leading researcher
Mikhail Batin
Founder
Anastasia Shubina
Creative concept developer
Azur James
Translator
Contacts
15260 Ventura Blvd, STE 2230, Sherman Oaks, CA 91403. Open Longevity department