TBDS addresses one of oncology's most critical unsolved problems — multidrug resistance — with a physically irreversible mechanism that no cancer cell can evolve around.
"TBDS exploits a fundamental vulnerability shared by nearly all solid tumors — overexpressed MMP-2/9 — to deliver an MDR-proof cytotoxic payload directly at the tumor site. No mutation, no efflux pump, no resistance pathway escapes physical membrane destruction."
The oncology drug market is enormous and still growing, yet treatment failure due to multidrug resistance remains the leading cause of cancer death. Existing approaches — ADCs, checkpoint inhibitors, targeted therapies — all rely on molecular mechanisms that cancer cells can evolve around.
TBDS takes a fundamentally different approach: physical membrane perforation. This mechanism is irreversible, independent of MDR machinery, and applicable across multiple solid tumor types simultaneously.
Interspace Biosystems has validated this approach in multiple in vitro and in vivo studies — demonstrating comparable or superior efficacy to trastuzumab (breast cancer) and docetaxel (prostate cancer) at equivalent doses, with no body weight loss.
Physical membrane perforation is independent of all known resistance mechanisms — P-glycoprotein overexpression, DNA repair upregulation, anti-apoptotic signalling. Cancer cells cannot evolve around physical lysis.
Zero cytotoxicity until MMP-2/9 cleavage. Healthy tissue, lacking elevated MMP expression, is spared. This is not reduced toxicity — it is abolition of off-target effects, confirmed in vitro.
No body weight loss observed in any TBDS-treated xenograft group, versus docetaxel at equivalent dosing. This safety profile is fundamental to the platform's clinical translatability and patient quality of life.
Tumor cell lysis releases damage-associated molecular patterns (DAMPs), priming anti-tumour immune responses. TBDS synergises with checkpoint inhibitors — opening combination therapy opportunities in the booming immuno-oncology market.
Single recombinant protein expressed in E. coli with a 3-step chromatography purification process. No complex conjugation chemistry, no ADC linker instability — straightforward scale-up pathway to commercial supply.
The core TBDS architecture is modular. ISB-22 demonstrates that new targeting moieties (anti-EGFR nanobody) can be fused to create new constructs targeting entirely new indications — without redesigning the platform from scratch.
TBDS is at the optimal inflection point for partnership — proof-of-concept in hand across multiple tumor types, but ahead of the cost-intensive IND and clinical stages.
Early partners gain access to a platform with validated in vivo data, a clear path to the clinic, and the broadest possible terms before Phase 1 data drives valuations higher.
~300K new US cases per year. TBDS (ISB-21) equalizes trastuzumab in HER2+ xenograft. TNBC — the hardest-to-treat subtype — remains particularly vulnerable to the physical lysis mechanism.
~288K new US cases per year. TBDS equalizes docetaxel efficacy in mCRPC xenograft with zero body weight loss. Represents a major tolerability advance for a disease requiring prolonged treatment.
~150K US cases per year. Dual targeting: TBDS TME activity plus ISB-22 EGFR-directed delivery bypasses RAS-mutation resistance to cetuximab — addressing a major unmet clinical need.
~235K US cases per year. EGFR mutations in 10–15% of NSCLC. ISB-22 targets this population plus EGFR-overexpressing tumors without mutation — a large addressable population beyond TKI therapy.
~66K US cases per year. 90%+ of HNSCC overexpresses EGFR. Resistance to cetuximab is highly prevalent — TBDS's physical mechanism provides a direct bypass, representing a strong second-line opportunity.
Connect with Interspace Biosystems to receive full scientific documentation, xenograft data packages, and to schedule a discussion with the founding team.