Dr. Dimitri Scherbakov
Co-founder, Lead Researcher, CEO
Over 25 years of experience in biochemistry / molecular biology, 15 years of drug development.
4 years of biotech experience.
h-index · to be confirmed LinkedIn
Restoring protein translation fidelity to prevent neurodegeneration at its source.
Preventing toxic protein misfolding before it starts
Transfidelity develops first-in-class small molecules that upgrade the accuracy of ribosomes in aging neurons — reducing the misfolded proteins that drive Parkinson’s and Alzheimer’s disease.
The problem
Neurodegeneration driven by toxic protein folding
As the brain ages, its protein quality-control systems become overwhelmed. Misfolded and aggregated proteins accumulate silently for years, ultimately driving Parkinson’s, Alzheimer’s, and other dementias that current drugs can only partially manage.
55M+
people live with dementia worldwide
Global costs already exceed US$1.3 trillion a year and are projected to reach US$2.8 trillion by 2030.
8.5M+
people with Parkinson’s disease (2019)
Prevalence has roughly doubled over the last 25 years.
0
disease-modifying therapies in wide use
Parkinson’s care runs into the tens of billions of dollars a year, yet no broadly effective treatment changes the course of disease.
The approach
A preventive, upstream approach: translation fidelity
Instead of trying to clear aggregates after neurons are already damaged, Transfidelity selectively increases the accuracy of ribosomal decoding in aging cells. Fewer translation errors mean fewer misfolded proteins, less proteostatic stress, and a chance to intervene before irreversible neurodegeneration takes hold.
Decoding accuracy
Aging neuron
CCU GAA GUC ACG misfolded ✕
+ Transfidelity
CCU GAA GCC ACG native fold ✓
Small molecules raise the fidelity of codon reading, so the right amino acid is incorporated and proteins fold correctly.
Key results
Measured in cells and in patient-derived neurons
20–25%
fewer translation errors
Lead compounds cut stop-codon readthrough and misincorporation by roughly 20–25% in mammalian cells — with no detectable global translation inhibition.
2 models
proteostasis rescued
In HEK293 and neuronal cell models, both lead compounds improve proteostasis-sensor readouts and reduce aggregation of endogenous and exogenous proteins.
3× SNCA
α-synuclein aggregates reduced
In iPSC-derived neurons from Parkinson’s patients with a 3× SNCA genotype, the compounds significantly reduce toxic alpha-synuclein aggregates.
Team
Team
A founder team with decades of ribosome and proteostasis research, joined by operational leadership to translate fidelity science into neuroprotective therapies.
Dr. Rashid Akbergenov
Co-Founder, Lead Researcher, CTO
Over 25 years of experience in biochemistry / molecular biology, 15 years of drug development.
4 years of biotech experience.
h-index · to be confirmed LinkedIn
Lorenzo Sacchetti
Founder Associate, BizDev
Saïd Business School, University of Oxford.
Project Management, Communications, AI support.
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Backed and supported by
- University of Basel
- University of Zurich
- Venture Kick
- Molecule
- Cerebrum DAO
- VitaDAO
Let’s talk about disease-modifying neuroprotection
Transfidelity is expanding its preclinical Parkinson’s program and exploring collaborations for hit-to-lead optimization, pathway mapping, and early development. Investors, pharma partners, and DeSci community members working on neurodegeneration are invited to get in touch.
Contact us
Prefer email? info@transfidelity.com