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Senescence Panel

For Senolytic Therapy

Senescence associated-β-galactosidase (SA-β-gal), SASP (IL-6, IL-8, IL-1β and TNFα) and NAD.

$698.00

SA-beta-gal

Cellular senescence is an important hallmark of aging. Senescent cells are so called zombie cells that stopped dividing but are not dead. Senescent cells do play important physiological functions including wound healing and slowing cancer progression, excessive senescence is mostly bad for healthy organ function and is believed to be one of the major causes of aging and shorten healthspan. There are more senescent cells in aged persons and in patients with many diseases including cancer, diabetes, kidney diseases and inflammatory diseases. Eliminating the excessive senescent cells (senolytic therapy) is believed to be an important anti-aging tool and can improve patient care outcome in many disease conditions.

Senescent cells release a variety of molecules that can change the function of not only neighboring cells but also remotely. Senescent cells can produce and release some 4000 different proteins, many of which have pro-inflammatory properties such as cytokines and chemokines. These molecules are call senescence-associated secreted phenotype (SASP) molecules that circulate in the blood stream. Different senescent cells can release a different subsets of SASP proteins. However, almost all senescent cells are believed to produce a lysosomal isoform of the beta galactosidases, commonly known as senescence-associated beta galactosidase (SABG or simply beta-gal). Many senescent cells also produce cell cycle proteins such as p16 and p53. More recently a lipid molecule, known as dihomo-15d-PGJ2, has been shown to be specifically produced by senescent cells.

In research studies, senescent cells are usually identified using cell staining for beta-gal. It is more challenging to assess the senescence burden in humans because of limited access to tissues at pathologic sites. We have conducted extensive studies and demonstrated the potential of SABG to assess the senescence burden in the whole body by analyzing the activity of lysosomal beta galactosidase in the serum, which are primarily released from dead or dying senescent cells allover the body. We showed that SABG in serum is highly increased in cervical cancer patients probably due to the activation of p53 by HPV infection. We have also demonstrated that a panel of SASP serum proteins predict the survival and response to therapy in cervical cancer. We also have preliminary data showing that SABG activity in serum from human subjects can be dramatically reduced by senolytic agents such as quercetin, suggesting that our SABG assay can potentially be used to monitor therapeutic response to senolytic therapy. The utility of SABG can be enhanced by adding a selected number of SASP proteins.

In our Senescence Panel, we measure serum SABG, four SASP proteins (IL-6, IL-8, IL-1b and TNFa) in serum, and intracellular NAD (icNAD). Inclusion of icNAD provides very important information because we have data showing that age management treatment such as senolytics may only be effective in individuals with optimized NAD level. Therefore, we recommend optimization before senolytic therapy or simultaneous treatment with NAD supplements and senolytics.

For researchers and age management clinics, Jinfiniti is pleased to work with you to reconfigure the most suitable set of senescence biomarkers and other longevity biomarkers to accomplish your goals.

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