Longevity has gone from fringe to focus in the past five years. But making drugs to combat a slow process is, well, slow. Meet Post-Translational Medicines. They developed proprietary disease models that speed up the aging process – and use high speed proteomics to identify protein states that were previously undetectable. 

Already, they’ve discovered many age-specific protein forms that can be drugged. One such program focuses on the lysosome – the cell’s waste disposal center. Reduced lysosomal function drives a lot of disease – and they’ve designed drugs to restore its activity, which can unlock new treatments in neurodegeneration and beyond.

This interview took place in January 2026 with co-founders Bryan Ngo (CEO) and Kevin Scott (Director of Discovery Chemistry).

Q: What new dimension does Post Translational Medicines bring to drug discovery?

Bryan Ngo:

Over the past decade, conventional precision medicine has targeted proteins that have specific mutations, which changes the protein’s shape, presenting new druggable pockets.  But other biological changes, not as immediately detectable as a genetic mutation, can also change the shape and function of a protein.

And this is where a lot of important biology happens, especially in aging. At Post Translational Medicines, we have developed methods to systemically identify these different protein states, known as proteoforms, and connect them to the aging processes. This tells us where to focus our drug discovery efforts.

Q: Aging is slow. How do you study it at speed?

Bryan Ngo:

We address the slow nature of aging by focusing on a core paradigm: aging is the result of the accumulation of maladaptive cellular states called senescence, or “zombie cells.”

At PTM, we’ve accelerated the drug discovery process for age-related diseases with our proprietary models and tools. This includes cellular models but also animal models whereby we can turn on and off aging like a light switch. 

Now, we can find out what really changes for example, in an aged or senescent neuron or hepatocyte, which proteins change their expression levels or muscle cells. Using these tools and approaches we are building the world’s first Aging Atlas of Druggable Proteoforms.

Q: What role do lysosomes play in cell aging?

Kevin Scott:

Lysosome dysfunction is considered a Hallmark of Aging.

Under normal, healthy conditions, lysosomes maintain cellular homeostasis by acting like the cell’s “trash disposal” or recycling center and removing toxic cellular waste products like proteins, metabolites, and lipids.

In aging, however, these lysosomes become less functional and less active. Buildup of waste clogs the cells and causes disease. In neurons, this was waste accumulation leads to protein aggregation and neurodegeneration diseases like Alzheimer’s. In muscles, loss of lysosome function is linked to sarcopenia or loss of muscle mass. This is a key driver of the overall aging proces sand leads to aging related diseases. 

Q: How do you fix damaged lysosomes? 

Bryan Ngo: 

The key to fixing damaged lysosomes is to restore their ability to acidify. 

In healthy cells, a large protein complex called the lysosome v-ATPase acts as an acid pump, pushing protons (acid) into the lysosome to keep the interior highly acidic. This acidity is essential for breaking down cellular waste. And with aging, this pump becomes dysfunctional.

Kevin Scott:

We’ve developed a novel therapeutic approach that focuses on restoring this core mechanism. Specifically, we’ve identified a powerful tool compound, PTM001, which reactivates one of these key proton pumps.

We believe we can address many, or even all diseases driven by lysosomal dysfunction. In neurodegeneration, this is relevant to Alzheimer’s, Parkinsons, frontotemporal dementia, ALS, Tay Sachs – one solution can impact them all. 

Q: How much progress have you made?

Bryan Ngo:

We’re an eight-month-old company, so we’ve been moving really really fast.

Kevin Scott:

We’ve designed and developed over 50 second-generation analogs for our lysosome program. Most importantly, we’ve already shown in cellular assays using tool compounds that we can selectively restore lysosome activity in aged cells.

This selective targeting of the dysfunctional cell types is a unique opportunity for us. It means that we can restore homeostasis and avoid the potential off-target toxicity you might see from simply turning on lysosome activity across all cells. Next is to test these analogues in cellular models of disease and moving to mouse testing next.

Q: Why are you confident you’re close to finding an asset to move forward with? 

Bryan Ngo:

 Because our tool compound already has very good data, I think we’re very close.