Expanding Disease Indications for JUV-161

In this Pharmaceutical Executive video interview, Hanadie Yousef, PhD, co-founder and CEO of Juvena Therapeutics, and 2023 Pharmaceutical Executive Emerging Pharma Leader, discusses Juvena’s fusion protein JUV-161, which enhances muscle regeneration and metabolism by AKT signaling. JUV-161 targets myotonic dystrophy type one and other muscle-wasting diseases. Juvena is also developing JUV-112 for obesity, targeting adipose tissue without appetite suppression and muscle loss. She also addressed how their platform uses quantitative proteomics and artificial intelligence to identify and validate proteins for therapeutic use.

Pharmaceutical Executive: JUV-161 is described as "pipeline in a product," with plans to broaden to other disease indications. Could you elaborate on the specific disease indications Juvena is targeting beyond myotonic dystrophy type one and the rationale behind prioritizing these expansions?

Hanadie Yousef: JUV-161 is a fusion protein Juvena discovered by mining proteins secreted by stem cells in order to identify proteins that have therapeutic tissue restorative effects, validate, and translate them into engineered biologics. JUV-161 was one of the first proteins that came out of the platform we built, where it acts to enhance muscle regeneration, improve muscle differentiation and muscle metabolism; ultimately leading to improvement in muscle health, and over time, strength and function. It acts by activating and restoring AKT signaling, which is dysregulated in the context of multiple muscle-wasting diseases and is dysregulated and down regulated during the natural aging process in people.

Because of this mechanism of action, JUV-161 as a fusion protein, a modified form of the human IGF2 protein, endogenously acts on muscle health and muscle function. Because of its natural mechanism of action, we've shown and validated that it has efficacy across multiple pre-clinical myopathy models, ranging from natural age-related muscle-wasting in a sarcopenia model through to glucocorticoid induced atrophy.

With its broad applicability, we're really excited about the potential to develop and commercialize it towards many indications in which it can restore muscle health and ultimately lead to restoring the quality of life for individuals. Some of the indications we're going to go after, after myotonic disorder type one, include potentially things like sarcopenia associated with aging, obesity, or even diabetes. The plan is to focus exclusively on showing proof of concept in myotonic dystrophy type one, due to the underlying cause of the disease, and AKT dysregulation is one of the hallmarks of what is driving some of the muscle wasting that people suffering this dystrophy are affected by.