Timeless Biosciences
Restoring the gut.
Protecting the patient.
Timeless Biosciences develops microbiome-derived therapeutics to overcome chemoresistance and alleviate gastrointestinal mucositis in patients undergoing treatment for colorectal cancer.
Our work begins where standard supportive care ends — at the interface of the gut epithelium, the resident microbial community, and the cytotoxic agents intended to cure disease but which too often disable the very tissue they pass through.
A microbe that blunts the cure.
Colorectal cancer is the second leading cause of cancer death worldwide, and a growing body of evidence points to a single tumor-resident bacterium — Fusobacterium nucleatum — as a central driver of resistance to the cytotoxic regimens used to treat it.1 F. nucleatum enriches in colorectal tumors, shelters within the tumor microenvironment, and engages host autophagy and innate-immune pathways in ways that allow malignant cells to survive 5-fluorouracil, oxaliplatin, and related agents.
The same axis carries a second toxicity. Fluoropyrimidines, irinotecan, and oxaliplatin disrupt the intestinal epithelium and reshape the resident microbial community, while bacterial enzymes — most notably β-glucuronidase — reactivate drug metabolites in the lumen and drive chemotherapy-induced diarrhea and mucositis.2 For many patients the result is dose reduction, delay, or outright discontinuation of therapy.
The result is a self-reinforcing loop in which the microbiome both amplifies drug toxicity and blunts drug efficacy. Despite five decades of clinical use, no therapy has been approved that directly addresses this axis. Supportive care remains palliative; dose-modification remains the default. We believe this is the wrong ceiling to accept, and that the molecules to break it already exist — made not by us, but by the microbes that share the patient's gut.
Three axes, one molecule.
- i. Recondition the tumor microenvironment Targeting F. nucleatum-driven signaling in colorectal tumors restores cancer-cell sensitivity to cytotoxic and immune-based regimens, addressing chemoresistance at its source rather than after the fact.
- ii. Suppress microbial drug reactivation By selectively constraining bacterial β-glucuronidase activity, the program limits luminal regeneration of toxic chemotherapy metabolites without disturbing the broader commensal community.
- iii. Restore the epithelial barrier Postbiotic activity preserves tight-junction integrity and supports crypt regeneration in the small intestine and colon, reducing the mucosal damage that drives clinical mucositis.