In this episode of Denatured, you&#x27;ll hear from Mark Lowdell, CSO &amp; co-founder at INmuneBio Inc. and Vishwas Seshadri, CEO &amp; director at Abeona Therapeutics. We examine how recessive dystrophic epidermolysis bullosa serves as a model for cell and gene therapy, and what this ultra-rare disease teaches us about scaling advanced treatments for the future. Host Jennifer C. Smith-Parker, Director of Insights, BioSpace Guests Mark Lowdell, CSO &amp; Co-Founder, INmuneBio Inc Vishwas Seshadri, CEO &amp; Director, Abeona Therapeutics Disclaimer: The views expressed in this discussion by guests are their own and do not represent those of their organizations.

From fragile skin to living medicine: Lessons from RDEB

BioSpace

# Full Transcript

**Podcast:** BioSpace

## Participants

- **Jennifer Smith-Parker** (BioSpace)
- **Mark Lowdell** (INmuneBio Inc)
- **Vish Sasadri** (Abeona Therapeutics)

## Transcript

Hi, my name is Jennifer Smith-Parker, Director of Insights at BioSpace, and you're listening to Denatured. In this episode, you'll hear from Mark Lodeau, CSO and co-founder of ImmuneBio, and Vishwas Sasadri, CEO and Director of Abiona Therapeutics. We explore how recessive dystrophic epidermolysis bullosa has become a defining case study for cell and gene therapy

and what this ultra-rare disease reveals about immune risk, manufacturing complexity, and the future scalability of advanced therapies. Hi Vish and hi Mark, thank you so much for joining this episode of Denatured. If you can please introduce yourselves, that would be great.

I'm Mark Lodeau, I'm the Chief Scientific Officer of ImmuneBio, a card-carrying immunologist and cellular therapist since the 1980s and the inventor of the drug we're going to talk about today, which is to treat the pediatric recessive dystrophic epidermolysis bullosa, or RDEB, as we prefer to call it. Thank you Mark. Hi everyone, I'm Vish Sasadri. I'm the President and CEO and Board Director at Abiona Therapeutics.

We're a cell and gene therapy company and our FDA-approved product in the disease space of RDEB, which is patients' own skin with genetic modification to produce collagen 7. So, I'm very excited to talk about the disease as well as the solutions we're trying to develop for that. Perfect. So, that's a great introduction, gentlemen. So, let's go ahead and start for our audience just to describe RDEB in the sense of what it is and what are its symptoms

and how basically from my understanding what a terrible disease it is. Yes. So, as Vish just said, it's due to a selective mutation or loss of collagen 7a, which is one of the critical proteins anchoring the dermis and epidermis at the dermal-epidermal junction. But it's a problem beyond the skin. It's a systemic problem. So, the symptoms they have in the skin, which is sloughing, the slightest trauma causes the epidermis to slough from the dermis.

They get blistering. But they get up their nose, behind their eyes, down their esophagus. And so, these children suffer tremendous pain and distress through the dressings that they need for skin. But they also then have these problems of failure to thrive because their gut doesn't work. And a lot of them get strictures because of the formation of fibrosis. And some of these are esophageal strictures. So, they may end up having to have esophageal dilatation procedures to every two or three weeks,

some of the children that I've seen in London. So, it is a very, very debilitating disease. And the median survival for RDEB patients, and RDEB being the worst of the conditions that form Epidermolysis Bullosa, but the median survival is mid-20s and many of these patients die of squamous cell carcinoma. So, some major problems that n...

From fragile skin to living medicine: Lessons from RDEB

Transcript

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From fragile skin to living medicine: Lessons from RDEB

Transcript

Built for investment professionals

Every day you wait, your competitors are findingedge in conversations you're not hearing.

Every day you wait, your competitors are finding
edge in conversations you're not hearing.