Preclinical-stage biotechnologyEarly-stage biotech company
A new class of dual-action, low-toxicity medicines designed to stop cancer growth, reactivate the immune system and minimize side effects.A new kind of medicine designed to stop cancer growing, help the immune system fight back and minimize side effects.
See how it worksSee how it works
Up to 70%
of human cancers have elevated or deregulated MYC.of human cancers have too much MYC activity.
0
MYC-targeted therapies with proven clinical benefit so far.therapeutics aimed at MYC that have been shown to help patients so far.
24+ years
of MYC research data from the Felsher lab at Stanford, behind our AI scientist.of MYC research from the Felsher lab at Stanford, which our AI assistant learns from.
The problem
01
MYC encodes a transcription factor whose aberrations, or upregulation of MYC-related pathways, occur in the vast majority of human cancers.MYC is a gene that acts like an accelerator for cell growth. In most human cancers, MYC or the systems it controls are stuck in overdrive.
02
In preclinical models, lowering MYC below a threshold level can cause tumor regression, a dependence known as oncogene addiction, and suppressing MYC can help restore the immune response against the tumor.In lab and animal studies, turning MYC down below a certain level can make tumors shrink. Lowering MYC can also help the immune system attack the tumor again.
03
Decades of effort have not yet produced a MYC-targeted therapy with demonstrated clinical efficacy.Scientists have tried for decades. No therapeutic aimed at MYC has yet been shown to work in patients.
Our approachHow it works
Our medicines are designed to partially silence MYC, enough to slow tumor growth and reactivate the immune response.Our medicines are designed to turn MYC down partway, not off. That is meant to be enough to slow the tumor and wake up the immune response.
01
Package.Pack.
Our delivery platform binds and protects the siRNA.The carrier wraps and protects the medicine.
02
Release.Deliver.
Inside the cell, the platform releases its cargo.Once inside a cell, the carrier lets the medicine go.
03
Dial down.Turn down.
The siRNA is designed to partially reduce MYC RNA.The medicine tells the cell to make less MYC, not zero.
Cartridge pairs anti-MYC siRNA, building on Dean Felsher's MYC research at Stanford, with the Cartridge Delivery Platform, built on biodegradable RNA carriers from Robert Waymouth's group at Stanford.We combine two lines of Stanford research: Dean Felsher's work on MYC, and biodegradable carriers from Robert Waymouth's group that carry genetic medicines into cells. We call this carrier the Cartridge Delivery Platform.
Cartridge Therapeutics is an AI-native therapeutics company developing siRNA medicines designed to partially silence the MYC oncogene, founded on research from Stanford University.Our medicines are made of short pieces of genetic material that tell a cell to make less of MYC. They are designed to turn MYC down partway, not off. The work started at Stanford University, and we use AI throughout.
Dual actionTwo jobs at once
Blocks tumor growth.Slows the cancer.
Designed to lower MYC below what tumors need to grow.Designed to lower MYC below the level a tumor needs to keep growing.
Reactivates immune response.Helps the immune system.
Designed to lower the CD47 and PD-L1 checkpoints that shield tumors.Designed to reduce the “don’t attack me” signals tumors use to hide from the immune system.
Based on Shachaf et al., Cancer Research, 2008 and Casey et al., Science, 2016.
AI-native therapeutics developmentBuilt with AI
01
We are building an AI scientist trained on more than 24 years of proprietary MYC research data and proprietary observations from the Felsher lab at Stanford.We are building an AI assistant that learns from more than 24 years of the Felsher lab’s own MYC research data and observations at Stanford.
02
We are developing digital twins, computational models of tumors and patients, to help design and prioritize experiments.We are building computer models of tumors and patients to help decide which experiments to run first.
03
We are building AI support across the pipeline, from discovery through preparing U.S. FDA filings.AI supports our work from the first experiments through preparing filings for the FDA, the U.S. agency that approves new medicines.
Lead programFirst target
TNBC lacks the estrogen, progesterone and HER2 receptors that many breast cancer therapies target, and it has the poorest outcomes of the breast cancer subtypes.Many breast cancer therapeutics work by locking onto one of three markers on the tumor. “Triple-negative” breast cancer has none of them, so those therapeutics do not work, and it has the worst outcomes of any breast cancer type.
MYC signaling is disproportionately elevated in triple-negative tumors compared with receptor-positive breast tumors.These tumors also tend to have much more MYC activity than other breast cancers.
Platform
Potential future indicationsOther cancers we could pursue
Our delivery platform is designed to carry anti-MYC siRNA, so the same approach could potentially extend well beyond our lead program.Because MYC is overactive in so many cancers, the same medicine and carrier could potentially help well beyond breast cancer.
A delivery platform, not a single therapeutic, aimed at MYC, which is elevated or deregulated in up to 70% of human cancers.This is a delivery platform, not a single therapeutic. MYC is overactive in up to 70% of human cancers.
Based on Dang, Cell, 2012 and Dhanasekaran et al., Nature Reviews Clinical Oncology, 2022.
Our biodegradable carriers break down into neutral small molecules, with no observable toxicity in mice, and partial silencing is designed to avoid shutting MYC off in normal cells.Our carriers break down in the body into small, inactive molecules, with no observable toxicity in mice. And because the medicine is designed to turn MYC down partway, not off, it aims to leave healthy cells enough MYC to work normally.
Based on Haabeth OAW, et al., PNAS, 2018 and Blake TR, et al., Bioconjugate Chemistry, 2023.
Team
Scientific co-founder and advisor
Professor of Medicine (Oncology) and of Pathology at Stanford University School of Medicine, and Director of Translational Research and Applied Medicine (TRAM). His lab studies how oncogenes such as MYC initiate and maintain cancer.
Scientific co-founder and advisor
Robert Eckles Swain Professor of Chemistry at Stanford University and, since 2026, a member of the National Academy of Sciences. He co-discovered the RNA delivery chemistry behind the Cartridge Delivery Platform.
Clinical co-founder
Executive Vice President and Chief Medical Officer of Caris Life Sciences. A breast cancer specialist, he was Chief of the Division of Oncology at Stanford (2013–2020) and President of the American Society of Clinical Oncology (2010–2011).
Business lead, SIC Venture Studio
Leads company building, operations and fundraising for Cartridge Therapeutics through SIC Venture Studio.
The scientific papers behind this work are listed in the .
Stanford affiliations are listed for identification only and do not imply endorsement by Stanford University.
Contact
For investor, press, research and general inquiries, email us.