Overcoming Resistance · Atlanta, GA

Restoring the gut.
Protecting the patient.

Developing microbiome-derived therapeutics targeting Fusobacterium nucleatum-induced chemoresistance in colorectal cancer. Our lead candidate also addresses chemo-induced GI toxicity. Two unmet needs, one mechanistic platform.

TB-001 · Microbiome-Immunotherapy Axis
Gut microbiome Lymph node Tumor microenv.
Tumor Health
100%
Active T-Cells
0
Fuso. Shielding
None

A defined, scalable biologic.

β-glucuronidase modulation· Butyrate / HDAC inhibition· AhR / IL-22 axis· PXR / IPA axis· FXR / TGR5 via UDCA· Mucosal Treg / IgA support· GPR41/43 SCFA signaling· β-glucuronidase modulation· Butyrate / HDAC inhibition· AhR / IL-22 axis· PXR / IPA axis· FXR / TGR5 via UDCA· Mucosal Treg / IgA support· GPR41/43 SCFA signaling·
The problem

F. nucleatum shields tumors
from chemotherapy.

In colorectal cancer, Fusobacterium nucleatum colonizes the tumor microenvironment and drives resistance to chemotherapy, blocking treatment response and worsening patient outcomes.


Patients with high F. nucleatum burden face significantly reduced survival, yet no approved therapeutic targets this mechanism.

Our science Meet the team
Mechanistic targets · TB-001
β-glucuronidase modulation
Reduces intestinal SN-38 from irinotecan conversion
PXR / IPA axis
Barrier integrity & xenobiotic metabolism via indole-3-propionic acid
AhR / IL-22 via indoles
Mucosal immune homeostasis, epithelial regeneration
HDAC inhibition via butyrate
GPR41/43 signaling · mucosal Treg / IgA support
FXR / TGR5 via UDCA
Bile acid signaling · intestinal homeostasis