Chemo efficacy. Without the toxicity. Regardless of genetics.

New Path Molecular is developing drug conjugates to treat solid tumours, addressing a biomarker present across most solid tumours, independent of genetic profile.

Funding

Innovate UK-funded

Lead programme

Candidate selection
CRC & pancreatic cancer

Strategy

Genetic-alteration agnostic

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Development pipeline

Our programmes

PDC-1 advancing in two tumour types, with platform expansion planned.

Asset	Modality	Biomarker	Indication	Stage	Next milestone
PDC-1 Lead programme	Synthetic PDC SN-38 payload	Phosphatidylserine (PS)	Colorectal cancer	Candidate Selection	IND/CTA-ready Target: end H1 2028
PDC-1 Expansion	Synthetic PDC SN-38 payload	Phosphatidylserine (PS)	Pancreatic cancer	Candidate Selection	IND/CTA-ready Target: end H1 2028
PDC-2 Discovery	PS-targeting platform	Phosphatidylserine (PS)	Other high-PS solid tumours	Discovery	—

For detailed milestone schedules or formal diligence enquiries, please contact us directly.

Our approach

Synthetic chemistry where biologics cannot go

A pan-tumour biomarker. A modality gap. A synthetic solution.

A conserved, pan-tumour biomarker

Phosphatidylserine (PS) is exposed on cancer cell membranes across tumour types, regardless of genetics.

Unreachable by existing modalities

When there are no accessible binding sites for antibodies, PS is a high-value target that current drugs cannot exploit.

Solved with a synthetic PDC

PDC-1 binds to PS directly and only then releases an SN-38 payload, sparing healthy tissue.

Mechanism of action

How PDC-1 works

PS Exposure

Phosphatidylserine (PS) flips to the outer leaflet of the cancer cell membrane. Unlike healthy cells, where PS stays hidden on the inner leaflet, cancer cells expose it universally, regardless of genetic profile.

Normal cell vs cancer cell showing phosphatidylserine exposure on the outer membrane leaflet

PDC-1 Structure

PDC-1 is a synthetic drug conjugate with three components: a PS-selective binder (orange) that drives tumour accumulation, a proprietary linker (blue) activated by the tumour environment, and an SN-38 anti-cancer payload (green).

PDC-1 molecule showing orange PS binder, blue linker, and green SN-38 payload

Tumour Accumulation & Cleavage

PDC-1 binds exposed PS on the cancer cell surface and accumulates at the tumour. Enzymes in the tumour microenvironment then selectively cleave the linker, separating the payload from the binder and activating it on site.

PDC-1 binding to phosphatidylserine on the cancer cell membrane

Selective Cell Death

SN-38 activates at the tumour, delivering superior efficacy at a lower dose than standard-of-care irinotecan. No organ toxicity was observed in preclinical models. Healthy cells, lacking exposed PS, are completely spared.

SN-38 payload selectively destroying cancer cell while healthy cell is spared

Logic-Gated Toxicity Control

Logic-gated cleavage controls levels of payload outside the tumour to non-toxic levels. Where PS is not present and pH is non-tumour-like, the molecule is excreted before the payload can be deployed.

Logic-gated cleavage mechanism controlling payload release outside tumour environment

Risk profile

Risks? Addressed.

Technical risk

£900k of non-dilutive funding has already done the work. PDC-1 has demonstrated preclinical efficacy, a clean safety profile, and superiority over the standard of care before a single pound of investor capital is deployed.

Manufacturing risk

No cell lines. No fermentation. No cold chain. PDC-1 is chemically synthesised from commercial feedstocks via a short, convergent process. The chemistry is simple and scalable.

Regulatory risk

The payload has an established clinical record. The PS biomarker is already FDA-cleared for clinical trials. The trial design is simple and well validated. New Path is not asking regulators to accept anything novel.

Preclinical evidence

What the data show

Reproducible findings across colon and pancreatic cancer models.

Target Validation

PS exposure confirmed across tumour types

Independent groups have replicated PS exposure on cancer membranes regardless of genetic profile, validating the pan-tumour hypothesis.

In Vivo Efficacy

Efficacy at lower dose than standard of care

PDC-1 has demonstrated superior efficacy to irinotecan in colon and pancreatic cancer models, supporting IND/CTA-enabling studies.

Safety

No organ toxicity observed

No detectable toxicity across preclinical safety assessments of liver, kidney, or gut. This is in contrast to standard-of-care irinotecan.

Patent

IP filed

Patent application filed covering the PDC-1 drug conjugate series. Further details available under NDA.

Preclinical data only. Clinical safety and efficacy have not yet been established.