Transfidelity for Protein Stability

FIDEL

Neurosciences

Neurodegenerative diseases such as Alzheimer's Disease are devastating conditions that impact millions globally. These diseases are driven by the misfolding and aggregation of proteins, which lead to brain cell death and cognitive decline. To make matters worse, as we age our cells become more error-prone, resulting in more errors during protein printing, causing proteins to clump together and form aggregates. Project Transfidelity aims to solve this by improving the accuracy of protein printing, preventing toxic aggregates from forming. Led by Dr. Dimitri Scherbakov and Dr. Rashid Akbergenov, with over 50 years of combined experience in the lab, we have identified two molecules that may improve the efficiency of protein production, potentially preventing protein aggregates, hypothesized to cause dementia. Despite the significant research funding allocated to neurodegenerative diseases, current therapies continue to treat the symptoms caused by the protein aggregates, with little progress made to stop or reverse disease. We’re trying to go after a potential root cause - rather than trying to clear aggregates once they are there, we aim to prevent them from forming in the first place by reducing the production of faulty proteins. With a clear path towards developing novel intellectual property (IP) and an ever-growing target market, we believe we are poised to make an impact on neurodegenerative disorders and the way we age.

Owned by

0x907Bb…35680

Contract:

0x23121…BbE1e

Description

Project Transfidelity aims to solve this by improving the accuracy of protein printing, preventing toxic aggregates from forming. Led by Dr. Dimitri Scherbakov and Dr. Rashid Akbergenov, with over 50 years of combined experience in the lab, we have identified two molecules that may improve the efficiency of protein production, potentially preventing protein aggregates, hypothesized to cause dementia.

Despite the significant research funding allocated to neurodegenerative diseases, current therapies continue to treat the symptoms caused by the protein aggregates, with little progress made to stop or reverse disease. We’re trying to go after a potential root cause - rather than trying to clear aggregates once they are there, we aim to prevent them from forming in the first place by reducing the production of faulty proteins. With a clear path towards developing novel intellectual property (IP) and an ever-growing target market, we believe we are poised to make an impact on neurodegenerative disorders and the way we age.

Team

Dr. Rashid Akbergenov

Research Lead

Organisation

University of Basel

Experiment Cost

$242,540.00

Project Score

Technology Readiness Level

PRE-TRL

TRL 1

TRL 2

TRL 3

TRL 4

Hypothesis formulated

Basic principles observed

Technology concept formulated

Experimental proof of concept

Technology validated in lab

Rationale

The project has conducted experimental laboratory work demonstrating proof-of-concept for the mechanism of action (reduced translational errors, reduced reporter protein aggregation, maintained protein synthesis rates) in HEK293 cells. However, all experiments to date have been performed in simplified in vitro systems (immortalized cell lines with artificial reporter constructs) rather than disease-relevant models. The stem cell-derived alpha-synuclein model and iPSC-derived neuronal models that would demonstrate disease relevance are explicitly stated as under development or planned for future work, not yet completed.

Assessment

Low Confidence

RecommendationPROMOTE

Total Score3.80

Overall Assessment

Transfidelity demonstrates strong TRL 2 performance with a weighted score of 3.8/5.0. The project shows excellent therapeutic relevance with validated hit compounds reducing translational errors and protein aggregation while maintaining cellular function. Two drug candidates have emerged with favorable early safety profiles and no toxicity. The novel mechanism targeting upstream protein misfolding rather than downstream aggregation is scientifically compelling with literature support. Key gaps include: disease-relevant validation in iPSC neuronal models (planned for early 2026), formal IP strategy documentation, and mechanism of action elucidation currently underway. The project is progressing ahead of schedule and represents a potential first-in-class therapy in an uncontested mechanism space.

Weighted Score

Price of FIDEL

$0.00541

Project Progress

All updates

All categories

Timeline

Activity

Time	Type	$FIDEL	USD	ETH	From

Project Score

Technology Readiness Level

PRE-TRL

TRL 1

TRL 2

TRL 3

TRL 4

Hypothesis formulated

Basic principles observed

Technology concept formulated

Experimental proof of concept

Technology validated in lab

Rationale

Assessment

Low Confidence

RecommendationPROMOTE

Total Score3.80

Overall Assessment

Weighted Score

Therapeutic Relevance

Strong early experimental support for hypothesis with two hit compounds demonstrating statistically significant reductions in translational errors in HEK293 cells. Compounds reduce protein aggregation of reporter constructs while maintaining synthesis rates, reinforcing biological relevance. Published literature supports the link between translation fidelity and neurodegeneration. However, validation in disease-relevant neuronal models is still planned, not completed.

Therapeutic Optionality

The platform targets multiple neurodegenerative diseases (Alzheimer's, Parkinson's, related disorders) indicating some optionality. The proprietary assay platform may extend to other proteostasis disorders. However, specific alternative applications beyond neurodegeneration are not yet explored, and pathway profiling to identify new applications is still underway.

Intellectual Property

Proprietary dual-reporter assays developed for measuring translational errors represent potential IP. Two hit compounds have undergone chemical evaluation and red-flag analysis, positioning them for IP protection. No competing translational fidelity modulators in clinical development suggests freedom to operate. However, no mention of formal patent filings or IP strategy in the documents.

Utility Of Candidates

Two viable hit compounds emerging with demonstrated activity: reduced translational errors, maintained protein synthesis, reduced reporter protein aggregation, and no cellular toxicity. Chemical evaluation and red-flag analysis completed. Compounds are progressing toward hit-to-lead optimization. However, efficacy in disease-relevant models (iPSC neurons) not yet demonstrated.

Prospects For Safety

Early safety signals are encouraging: compounds show improved proteostasis without cellular toxicity in HEK293 cells, and critically maintain overall protein synthesis rates (avoiding global translation suppression). Red-flag analysis completed on compounds. No toxicity concerns reported. However, more comprehensive safety profiling in disease-relevant models and in vivo studies not yet conducted.