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Eliminating Senescent Cells by Activating the Immune System (Robin Mansukhani, Deciduous Therapeutics)

Eliminating Senescent Cells by Activating the Immune System (Robin Mansukhani, Deciduous Therapeutics)

FromTranslating Aging


Eliminating Senescent Cells by Activating the Immune System (Robin Mansukhani, Deciduous Therapeutics)

FromTranslating Aging

ratings:
Length:
44 minutes
Released:
Jun 8, 2022
Format:
Podcast episode

Description

This week’s episode of Translating Aging features Robin Mansukhani, CEO and Co-founder of Deciduous Therapeutics, a company that aims to positively impact human healthspan by developing medicines which activate the endogenous immune mechanism responsible for the elimination of senescent cells. Today, Robin shares his insights on how senescent cells develop and how Deciduous Therapeutics eliminates them.
Robin begins by explaining what causes the growth of senescent cells. He explains that not all senescent cells are dangerous and discusses the various kinds of these cells. Although senescent cells are prominent in age-related diseases, Robin explains that they are also found in younger people with autoimmune diseases such as juvenile diabetes. He goes on to talk about Deciduous Therapeutics’ approach in combating senescent cells by activating the NKT cells. He also shares his thinking about the best directions for human trials. The episode concludes with Robin describing the future of Deciduous Therapeutics, and his focus on impacting people globally in a meaningful way.
In this episode, you’ll learn how senescence arises, traditional senolytic approaches, and the importance of NKT cells in eliminating these pathogenic celss.
Episode Highlights:
The origin of senescent cells

Why are senescent cells highly pathogenic?

Breaking down the different kinds of senescent cells

The relationship between senescent cells and age-related diseases

Senolytics and senostatics: approaches for getting rid of senescent cells

Deciduous Therapeutics’ approach

What happens when senescent cells overpower NKT cells?

The role alpha-galactosyl ceramide on NKT cells

The current hurdles Deciduous Therapeutics are trying to overcome

How Robin see Deciduous Therapeutics in five years

Quotes:
“Senescent cells are cells that have been irreversibly damaged, and so they exit the cell cycle.”
“It's not about the age of the person. It's more about the biological age of the organ and tissue. So we see senescence, also, in young people.”
“If you can take a senescent cell that's pathogenic and make it good again, and make it functional again safely and successfully, that would be very useful.”
“The approach here and our mindset going into creating this company was: there's a way that nature intended for this to happen, and it is our job to figure that out.”
“Getting the first indication to work means that you'll have a runway to lots of success. But if your first one does not work, in a lot of cases, it might mean the end of the company or the end of the runway because you simply don't get enough funding for multiple clinical trials at once. So it is critical.”
Links:
Email questions, comments, and feedback to podcast@bioagelabs.com
Translating Aging on Twitter:https://twitter.com/BioAgePodcast ( @bioagepodcast)
BIOAGE Labs Websitehttps://bioagelabs.com/ ( BIOAGELabs.com)
BIOAGE Labs Twitterhttps://twitter.com/bioagelabs?lang=en ( @bioagelabs)
BIOAGE Labshttps://www.linkedin.com/company/bioage-labs/ ( LinkedIn)
Deciduous Therapeutics Websitehttps://www.deciduoustx.com/ ( DeciduousTx.com)
Released:
Jun 8, 2022
Format:
Podcast episode

Titles in the series (51)

On Translating Aging, we talk with the worldwide community of researchers, entrepreneurs, and investors who are moving longevity science from the lab to the clinic. We bring you a commanding view of the entire field, in the words of the people and companies who are moving it forward today. The podcast is sponsored by BioAge labs, a clinical-stage biotechnology company developing therapies to extend human healthspan by targeting the molecular causes of aging.