The protein can end too early.
A nonsense mutation turns a sense codon into a premature stop. Translation may produce a shortened protein with reduced, absent or altered function.
INDIA-BUILT · PRECISION TRANSLATION THERAPEUTICS
Reading through
silence.
Restoring the protein.
Developing AI-guided suppressor-tRNA therapeutics.
For genetic messages that stop too soon.
THE MOLECULE AT THE HEART OF OUR MISSION
ONE RNA STRAND · A FOLDED ADAPTOR
A single RNA backbone folds into stems and loops. One end carries an amino acid; the other reads the message.
One strand. A remarkable fold.
01 / THE POSSIBILITYENGINEERING THE LANGUAGE OF LIFE
The message
is interrupted.
The possibility
is not.
WHY KRITRNA EXISTS
Our cells carry instructions for making proteins. Sometimes, a single mutation tells the cell to stop before the work is complete.
KritRNA is building a suppressor-tRNA therapeutics platform for selected nonsense-mutation contexts. We combine molecular biology, evidence-led programme selection and computational translation science to explore where restoring full-length protein could make a meaningful difference.
Understand the molecular challenge ↗DISCOVERY-LED. EVIDENCE-GUIDED. INDIA-BUILT.
02 / LEARN THE SCIENCEFROM THE MESSAGE TO THE PROTEIN
A cell reads its instructions
three letters at a time.
DNA stores the instructions. mRNA carries a working copy. The ribosome reads it. tRNA connects the code to the amino acids that build a protein.
A tRNA is a single RNA chain folded into an adaptor, with parts of the same chain paired into stems. One end carries an amino acid; the other helps recognise a codon on the message. At a normal stop, release factors end translation.
Normal translation
A ribosome reads mRNA in three-letter codons. Aminoacyl-tRNAs deliver amino acids; the growing chain is extended until release factors recognise a normal stop.
The highlighted CAG is a sense codon. The ribosome moves along the message from 5′ to 3′.
The message can be lost.
Nonsense-mediated decay can reduce the transcript before enough protein is made. Readthrough and message survival are connected questions that need to be studied together.
THE THERAPEUTIC IDEA
Help translation continue—without editing the DNA sequence.
Our approach acts during protein synthesis. Its duration, dosing and effects depend on how the candidate is designed and delivered.Scientific background: Reference tRNA structure ↗Published suppressor-tRNA research ↗
03 / WHAT HAS TO WORKCONNECTED CONDITIONS, NOT ISOLATED SCORES
Four conditions.
One biological context.
A molecule cannot succeed on design alone. Charging, termination competition, message survival and delivery have to be considered together.
Charging
Can the tRNA carry its intended amino acid?
A tRNA must be recognised and charged by an appropriate aminoacyl-tRNA synthetase. Recognition of a stop codon alone is not sufficient.
Termination competition
Can translation continue at the selected stop?
The suppressor tRNA competes with the machinery that normally ends translation. The local sequence and the state of the ribosome matter.
Message survival
Is there enough mRNA left to read?
Nonsense-mediated decay can reduce the available transcript. Its effect varies with the gene, transcript architecture and cellular context.
Delivery
Can the candidate reach the right cells?
A promising molecular design still needs a credible route to the relevant tissue and an effective intracellular exposure.
SAFETY ACROSS EVERY CONDITION
Useful protein function, normal-stop fidelity and cellular response matter alongside readthrough activity. They are part of the evidence—not optional checks at the end.
THE PLATFORMIN DEVELOPMENT · BUILT TO BE TESTED
Design the molecule.
Understand its world.
Making a candidate is one challenge.
Choosing the right one is another.
We are developing two connected engines to help make that choice more informed. One focuses on the candidate. The other considers the translation system it enters. Both are designed to learn from experiments.
ENGINE 01 / CANDIDATE DESIGN01
From a mutation
to a testable choice.
Engine 01 is being developed to explore suppressor-tRNA candidates in the context of a selected nonsense mutation. It brings molecular suitability and the intended restoration goal into a common decision process.
- Intended output
- An explainable candidate shortlist, its supporting evidence and the questions to test next.
- What earns confidence
- Prospective experiments in a relevant biological context.
ENGINE 02 / SYSTEMS THINKING02
BIOLOGY IS CONNECTED
Message availability, translation, quality control and protein output influence one another.
From one molecule
to connected consequences.
Engine 02 is a developing systems model of translation. It asks how a candidate may interact with message availability, ribosome behaviour, termination, quality control and the production of useful protein.
- Intended output
- Testable hypotheses about biological dependencies, potential bottlenecks and the measurements that matter.
- What earns confidence
- Experimental challenge and calibration—not an impressive network picture.
Design
Begin with the biological question.
Explore candidate possibilities for a defined mutation and intended protein-restoration goal.
Measure
Keep the experiment in context.
Assess readthrough alongside protein output, function, cellular response and effects at normal stop codons.
Rank
Make the next choice more informed.
Develop experimentally challengeable prioritisation with a clear rationale and explicit uncertainty.
Expand
Carry forward what the evidence supports.
Use each research programme to inform the next while recognising that delivery and disease biology remain programme-specific.
The engines support a design–test–learn programme. Functional protein restoration, delivery and safety are experimental questions, not outputs that a model can certify.
04 / RESEARCH PROGRAMMESEARLY RESEARCH · PROGRAMME DEFINITION
A shared error class.
Distinct biological questions.
A premature stop in a different gene can create a different disease. Our initial focus is selected nonsense-mutation contexts in HBB, DMD and TP53. Each programme has its own protein-restoration, delivery and safety questions.
01Hematology · India-priorityβ-ThalassemiaHBB
Design suppressor-tRNA candidates for selected HBB nonsense-mutation contexts and restore β-globin production.
CURRENT MILESTONE
Program definition
NEXT EVIDENCE GATE
Candidate design and in-vitro assay specification
02NeuromuscularDuchenne muscular dystrophyDMD
Design suppressor-tRNA candidates for selected DMD premature-stop contexts and restore full-length dystrophin.
CURRENT MILESTONE
Program definition
NEXT EVIDENCE GATE
Candidate design and reporter-assay specification
03Oncologyp53-deficient cancerTP53
Explore suppressor-tRNA strategies for selected TP53 nonsense mutations with the aim of restoring full-length p53 protein and tumour-suppressor function.
CURRENT MILESTONE
Program definition
NEXT EVIDENCE GATE
Mutation prioritisation and disease-relevant functional-assay planning
OUR ORIGIN. OUR PURPOSE.INDIA → GLOBAL SCIENCE
CREATED WITH PURPOSERooted in India.
Rooted in India.
Engineered to continue.
KritRNA brings together कृ (kṛ), the Sanskrit root meaning “to make, create or act”, and tRNA, the molecular adaptor that helps translate genetic information into protein. Together: tRNA created with purpose, engineered to help translation continue.
Our name expresses our ambition: to build scientific ownership in India and contribute original, rigorous biotechnology to the world. Our programmes connect molecular science, computational development and evidence generation with the realities of the people they may one day serve.
Scientific ownershipAccess-aware developmentGlobal collaboration
Read our founding story ↗05 / PEOPLE & PURPOSEOUR FOUNDING STORY ↗
Serious science.
Shared purpose.
KritRNA brings molecular research, computational ambition and patient-centred communication into one company. Our founders are building from India, with a scientific outlook that crosses borders.
Why we are building KritRNA ↗Our team and scientific network ↗
06 / THE SCIENTIFIC FOUNDATIONEXPLORE THE EVIDENCE HUB ↗
Ambition, grounded
in the evidence.
The better question is not only whether readthrough can happen. It is which candidate to test, in which context, and what evidence would justify the next step.
PUBLISHED ACADEMIC RESEARCH
Translation velocity determines the efficacy of engineered suppressor tRNAs on pathogenic nonsense mutations
Bharti, Santos, Davyt and colleagues
Nature Communications · 2024 · 15:2957
Nikhil Bharti and Leonardo Santos contributed equally. This published academic work is a scientific foundation, not validation of KritRNA’s developing platform.
Read the open-access paper ↗07 / FIND YOUR WAY INDIFFERENT PERSPECTIVES. ONE MISSION.
BUILD THE NEXT CHAPTERBetter questions.
Better questions.
Greater possibilities.
We welcome scientific, CRO, disease-model, delivery and strategic collaborators who want to turn a compelling biological idea into rigorous experimental evidence.