Restoring tumor suppression through genomic medicine.

Indel Bioinnovations is developing non-viral genomic medicines to restore the tumor-suppressor functions cancer has lost. Our lead program, INDEL-53, starts with p53.

Platform focusOne platform. A lead program in TP53-altered cancer.
Lead programINDEL-53
Lead indicationTriple-negative breast cancer (TNBC)
StagePreclinical
Therapeutic architectureINDEL-53
Restoring a lost cellular defenseThe INDEL-53 development strategy
01
DeliverNon-viral approach
02
ExpressFunctional p53
03
RestoreDamage response
Preclinical efficacy signal~75%
tumor growth inhibition relative to control in a TNBC xenograft model
Platform thesis

Restore a core tumor suppressor.

Cancer therapies often inhibit an overactive driver. Indel takes a different starting point: restoring a protective function that cancer cells have lost.

Skip to the preclinical evidence
Why the elephant matters

Nature offers a powerful clue.

Elephants show lower-than-expected cancer rates despite their large size and long lifespan.

Why more TP53 matters

Their expanded TP53 gene family contributes to a heightened DNA-damage response, helping damaged cells undergo apoptosis.

Abegglen et al., JAMA, 2015; Sulak et al., eLife, 2016.
01Before treatment

A critical cellular defense is lost.

TP53 encodes p53, a protein that helps cells respond to DNA damage. When its function is impaired, damaged cells can survive and continue dividing.

02During treatment

Introduce functional TP53.

INDEL-53 is designed to deliver functional human TP53 DNA into tumor cells through a non-viral system.

Sustained expression

Genomic integration is designed to support sustained TP53 expression, enabling cells to produce functional p53.

03After treatment

Re-engage the damage response.

The intended response is restored p53 activity that helps damaged cells stop dividing or undergo apoptosis, a controlled form of cell death.

Intended cellular responseExplore the preclinical evidence
Why TNBC

A concentrated biological opportunity with significant unmet need.

Triple-negative breast cancer (TNBC) tests negative for estrogen receptors, progesterone receptors, and HER2. These three biomarkers guide treatment in other breast cancer subtypes. TNBC’s aggressive biology and fewer receptor-directed treatment options create a significant unmet need.

~15%of breast cancers are triple-negativeNational Cancer Institute
~350Kestimated TNBC diagnoses worldwide each year2022 estimate · NCI / IARC
14.9%five-year relative survival for distant-stage TNBCNCI SEER · Female cases, 2016–2022
Biology-to-program fit~80%

TP53 is mutated in approximately 80% of TNBC tumors across published studies, creating a genetically concentrated entry point for INDEL-53.

Current treatment landscape

More options, but persistent limits.

Depending on stage and biomarkers, treatment may include surgery, chemotherapy, radiation, immunotherapy, antibody-drug conjugates, and selected targeted therapies.

Preclinical evidence

A clear early signal in a high-need indication.

INDEL-53 demonstrated antitumor activity in a preclinical TNBC xenograft study, supporting continued translational development.

In vivo TNBC xenograft model
~75%

Tumor growth inhibition

At Day 17, relative to vehicle control, with tumor growth normalized to each group’s baseline.

n = 12 per groupIn vivo · Preclinical
Tumor growth over the study
VehicleINDEL-53
Mean tumor volume in a preclinical TNBC xenograft studyMean tumor volume in the MDA-MB-231 TNBC xenograft model, with 12 animals per group. At days 0, 3, 6, 10, 13, 17, vehicle means were 196.8, 332.0, 460.1, 647.2, 904.5, 1065.9 cubic millimeters. INDEL-53 means were 196.4, 227.3, 227.3, 278.4, 351.9, 418.0 cubic millimeters. Error bars show plus or minus one standard error of the mean. Day 17 baseline-normalized tumor growth inhibition was 74.45%.Mean tumor volume (mm³)030060090012001500036101317Days after first dose
Mean ± SEM; n = 12 animals per group. MDA-MB-231 TNBC xenograft model.
Preclinical only

Clinical safety and efficacy have not yet been established.

Development path

An FDA-informed path toward the clinic.

Early regulatory engagement alongside a focused preclinical development program.

01
Platform

System development

Delivery optimization and therapeutic architecture.

02
Validation

Preclinical signal

Efficacy assessment across TNBC models.

03
Planned

Pre-IND & IND-enabling work

Safety, biodistribution, manufacturing development, and further regulatory interactions.

04
Future

Clinical translation

Initial clinical development in TNBC with expansion potential.

Planned stages remain subject to further development.

Platform horizon

One platform. A much larger vision.

INDEL-53 is the first application of a platform designed to restore the genomic functions cancer cells have lost.

01Today

INDEL-53

Restore functional TP53

TP53 alterations occur in approximately 50% of cancers. TNBC is the initial indication for INDEL-53, with a broader opportunity in tumors with impaired p53 function.

Lead program · Preclinical development
02Next

Beyond p53

Additional lost genomic functions

Explore whether the platform can support restoration of other tumor-suppressor functions and loss-of-function cancer drivers.

Future development concepts
03Longer term

Programmable genomic medicine

A broader therapeutic platform

Develop a flexible foundation for genomic medicines that address the protective functions lost across different cancers.

Long-term platform vision

Programs beyond INDEL-53 are future development concepts. They have not been clinically validated.

Our origins

From university research to independent development.

Founded by BYU-trained scientists and entrepreneurs, Indel Bioinnovations builds on technology originating in research at Brigham Young University.

Indel is now an independent biotechnology company directing its own research, business operations, and therapeutic development.

Provisional patent application filed in October 2026.

01
University researchA foundation in tumor-suppressor biology
02
Company formationIndel formed to advance cancer therapeutics
03
Independent developmentCompany-led therapeutic development with an industry-focused team
Team

Scientific depth. Industry experience.

A focused core team supported by industry, commercialization, and strategic advisors.

Core Team
Peyton Jackson

Peyton Jackson

Chief Executive Officer

BYU-trained in genetics and biotechnology and a former genetics lab manager. Leads company strategy, fundraising, and business development.

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Jared Wieland

Jared Wieland

Chief Scientific Officer

PhD student at BYU with more than six years of research experience and drug design training at OHSU. Leads scientific strategy and the preclinical advancement of INDEL-53.

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Jared Barrott

Jared BarrottPhD

Co-founder & Scientific Advisor

Cancer pharmacologist whose prior research includes postdoctoral work at Huntsman Cancer Institute at the University of Utah, guiding translational strategy and oncology model development.

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Industry & Strategic Advisors
Greg Kunst

Greg Kunst

Business Advisor

CEO of Valitor and former founder and CEO of Aurion Biotech, acquired by Alcon in 2025. Brings experience in company building, clinical development, and commercialization.

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Laurens Bouckaert

Laurens Bouckaert

Business Advisor

Independent biotech executive and advisor to INGENIA, with more than 20 years of commercial experience. Brings expertise in business development, market access, and growth strategy.

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Jon Sparks

Jon SparksPhD, JD

Strategic Advisor

Partner at McCarter & English with a PhD in biochemistry. Brings scientific and legal expertise to technology commercialization and long-term company strategy.

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Research contributors
Spencer NadauldResearch Assistant
Will PenrodResearch Team
Partner with Indel

Advance the next chapter of genomic medicine.

We welcome investors, strategic partners, and scientific collaborators interested in advancing INDEL-53 and exploring the broader platform.