# Cartridge Therapeutics (cartridgetx.com): page mirror Markdown mirror of https://cartridgetx.com/ for AI agents and text tools. It contains the same words as the website, in both of its versions: Science (default) and Plain English (https://cartridgetx.com/?v=plain). Short fact sheet: https://cartridgetx.com/llms.txt - Humans: use the contact section at https://cartridgetx.com/#contact - AI agents and automated inquiries: agents@sicventure.com --- # Science version **Preclinical-stage biotechnologyEarly-stage biotech company** ## Dialing down MYC, a cancer driver that has resisted conventional drugs. A new class of dual-action, low-toxicity medicines designed to stop cancer growth, reactivate the immune system and minimize side effects. Cartridge Therapeutics is an AI-native drug company developing siRNA medicines designed to partially silence the MYC oncogene, founded on research from Stanford University. A delivery platform, not a single drug, aimed at MYC, which is elevated or deregulated in up to 70% of human cancers. **The problem** ### MYC drives many cancers, yet it has no targeted therapy with proven clinical benefit. #### A central cancer driver. MYC encodes a transcription factor whose aberrations, or upregulation of MYC-related pathways, occur in the vast majority of human cancers. #### Tumors depend on it. 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. #### Long called "undruggable." Decades of effort have not yet produced a MYC-targeted therapy with demonstrated clinical efficacy. **Our approachHow it works** ### Dial down MYC at the RNA level, and solve delivery. 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. Our medicines are designed to partially silence MYC, enough to slow tumor growth and reactivate the immune response. - 01 Package. Our delivery platform binds and protects the siRNA. - 02 Release. Inside the cell, the platform releases its cargo. - 03 Dial down. The siRNA is designed to partially reduce MYC RNA. **Dual actionTwo jobs at once** Blocks tumor growth. Designed to lower MYC below what tumors need to grow. Reactivates immune response. Designed to lower the CD47 and PD-L1 checkpoints that shield tumors. Based on [Shachaf et al., Cancer Research, 2008](https://doi.org/10.1158/0008-5472.CAN-07-6192) and [Casey et al., Science, 2016](https://doi.org/10.1126/science.aac9935). **AI-native drug developmentBuilt with AI** ### We are building AI into how we develop medicines, from discovery to regulatory filings. #### An AI scientist. 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. #### Digital twins. We are developing digital twins, computational models of tumors and patients, to help design and prioritize experiments. #### Through regulatory filings. We are building AI support across the pipeline, from discovery through preparing filings with the U.S. Food and Drug Administration (FDA). **Lead programFirst target** ### Triple-negative breast cancer (TNBC) 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. MYC signaling is disproportionately elevated in triple-negative tumors compared with receptor-positive breast tumors. - Program: Anti-MYC siRNA - Stage: Preclinical research **Platform** ### One delivery platform, many MYC-driven cancers. Our delivery platform is designed to carry anti-MYC siRNA, so the same approach could potentially extend well beyond our lead program. **Lead programFirst target** Triple-negative breast cancer (TNBC) **Potential future indicationsOther cancers we could pursue** Liver cancer (HCC) · Lymphoma · Multiple myeloma · Prostate cancer Based on [Dang, Cell, 2012](https://doi.org/10.1016/j.cell.2012.03.003) and [Dhanasekaran et al., Nature Reviews Clinical Oncology, 2022](https://doi.org/10.1038/s41571-021-00549-2). #### Designed for low toxicity. Our biodegradable carriers break down into neutral small molecules that were well tolerated in mice, and partial silencing is designed to avoid shutting MYC off in normal cells. Based on [Haabeth OAW, et al., PNAS, 2018](https://doi.org/10.1073/pnas.1810002115) and [Blake TR, et al., Bioconjugate Chemistry, 2023](https://doi.org/10.1021/acs.bioconjchem.3c00019). **Team** ### Founders and team #### Dean W. Felsher, MD, PhD 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. #### Robert M. Waymouth, PhD 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. His group co-discovered the RNA delivery chemistry behind the Cartridge Delivery Platform. #### George W. Sledge Jr., MD 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). #### Paul Grewal Business lead, SIC Venture Studio Leads company building, operations and partnerships for Cartridge Therapeutics through SIC Venture Studio. Stanford affiliations are listed for identification only and do not imply endorsement by Stanford University. #### SELECTED PUBLICATIONS - Felsher DW. Cancer revoked: oncogenes as therapeutic targets. Nature Reviews Cancer, 2003. https://doi.org/10.1038/nrc1070 - Jain M, et al. Sustained loss of a neoplastic phenotype by brief inactivation of MYC. Science, 2002. https://doi.org/10.1126/science.1071489 - Shachaf CM, et al. Genomic and proteomic analysis reveals a threshold level of MYC required for tumor maintenance. Cancer Research, 2008. https://doi.org/10.1158/0008-5472.CAN-07-6192 - Rakhra K, et al. CD4+ T cells contribute to the remodeling of the microenvironment required for sustained tumor regression upon oncogene inactivation. Cancer Cell, 2010. https://doi.org/10.1016/j.ccr.2010.10.002 - Casey SC, et al. MYC regulates the antitumor immune response through CD47 and PD-L1. Science, 2016. https://doi.org/10.1126/science.aac9935 - Dang CV. MYC on the path to cancer. Cell, 2012. https://doi.org/10.1016/j.cell.2012.03.003 - Dhanasekaran R, et al. The MYC oncogene: the grand orchestrator of cancer growth and immune evasion. Nature Reviews Clinical Oncology, 2022. https://doi.org/10.1038/s41571-021-00549-2 - Smith BAH, et al. MYC-driven synthesis of Siglec ligands is a glycoimmune checkpoint. PNAS, 2023. https://doi.org/10.1073/pnas.2215376120 - McKinlay CJ, et al. Charge-altering releasable transporters (CARTs) for the delivery and release of mRNA in living animals. PNAS, 2017. https://doi.org/10.1073/pnas.1614193114 - Haabeth OAW, et al. mRNA vaccination with charge-altering releasable transporters elicits human T cell responses and cures established tumors in mice. PNAS, 2018. https://doi.org/10.1073/pnas.1810002115 - Blake TR, et al. Lysine-derived charge-altering releasable transporters: targeted delivery of mRNA and siRNA to the lungs. Bioconjugate Chemistry, 2023. https://doi.org/10.1021/acs.bioconjchem.3c00019 --- # Plain English version **Preclinical-stage biotechnologyEarly-stage biotech company** ## Turning down MYC, a gene that fuels many cancers and that existing drugs have not been able to reach. We are developing a new kind of medicine designed to do two jobs: stop cancer from growing and help the immune system fight back. It is designed for low toxicity, to minimize side effects. 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. This is a delivery platform, not a single drug. MYC is overactive in up to 70% of human cancers. **The problem** ### One gene helps fuel many cancers. No drug aimed at it has yet been shown to help patients. #### A growth accelerator. 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. #### Tumors depend on it. 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. #### Long out of reach. Scientists have tried for decades. No drug aimed at MYC has yet been shown to work in patients. **Our approachHow it works** ### Turn MYC down at the source, and get the medicine where it needs to go. 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. 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 Pack. The carrier wraps and protects the medicine. - 02 Deliver. Once inside a cell, the carrier lets the medicine go. - 03 Turn down. The medicine tells the cell to make less MYC, not zero. **Dual actionTwo jobs at once** Slows the cancer. Designed to lower MYC below the level a tumor needs to keep growing. Helps the immune system. 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](https://doi.org/10.1158/0008-5472.CAN-07-6192) and [Casey et al., Science, 2016](https://doi.org/10.1126/science.aac9935). **AI-native drug developmentBuilt with AI** ### We use AI at every step, from early research to the paperwork regulators need. #### An AI research assistant. 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. #### Virtual tumors. We are building computer models of tumors and patients to help decide which experiments to run first. #### All the way to the FDA. AI supports our work from the first experiments through preparing filings for the U.S. Food and Drug Administration (FDA). **Lead programFirst target** ### A hard-to-treat breast cancer Many breast cancer drugs work by locking onto one of three markers on the tumor. “Triple-negative” breast cancer has none of them, so those drugs do not work, and it has the worst outcomes of any breast cancer type. These tumors also tend to have much more MYC activity than other breast cancers. - What it is: A medicine that turns MYC down - Stage: Lab and animal research, before human trials **Platform** ### One delivery platform, potentially many cancers. Because MYC is overactive in so many cancers, the same medicine and carrier could potentially help well beyond breast cancer. **Lead programFirst target** Triple-negative breast cancer **Potential future indicationsOther cancers we could pursue** Liver cancer · Lymphoma (a blood cancer) · Multiple myeloma (a bone marrow cancer) · Prostate cancer Based on [Dang, Cell, 2012](https://doi.org/10.1016/j.cell.2012.03.003) and [Dhanasekaran et al., Nature Reviews Clinical Oncology, 2022](https://doi.org/10.1038/s41571-021-00549-2). #### Designed for low toxicity. Our carriers break down in the body into small, inactive molecules, which mice tolerated well. And because the medicine is designed to turn MYC down partway, not off, it aims to leave healthy cells enough MYC to work normally. The goal is to minimize side effects. Based on [Haabeth OAW, et al., PNAS, 2018](https://doi.org/10.1073/pnas.1810002115) and [Blake TR, et al., Bioconjugate Chemistry, 2023](https://doi.org/10.1021/acs.bioconjchem.3c00019). **Team** ### Founders and team #### Dean W. Felsher, MD, PhD 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. #### Robert M. Waymouth, PhD 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. His group co-discovered the RNA delivery chemistry behind the Cartridge Delivery Platform. #### George W. Sledge Jr., MD 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). #### Paul Grewal Business lead, SIC Venture Studio Leads company building, operations and partnerships for Cartridge Therapeutics through SIC Venture Studio. Stanford affiliations are listed for identification only and do not imply endorsement by Stanford University. The scientific papers behind this work are listed in the Science version above. Our medicines are still in research and have not been tested in people. Nothing on this site is medical advice. --- © 2026 Cartridge Therapeutics Our programs are investigational and preclinical. Nothing on this site is medical advice.