New Path Molecular | PS-targeted synthetic drug conjugates for solid tumours

Approach

Synthetic chemistry vs. biologics

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

A conserved, pan-tumour target

Phosphatidylserine (PS) is externalised on tumour cell membranes across tumour types, regardless of genetic profile. This externalisation is the targeting address NPMR-047 exploits.

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

NPMR-047 binds externalised PS and accumulates at the tumour. The tumour microenvironment contributes to cleaving the linker, releasing SN-38 on site. Both conditions must be met for payload release.

Pipeline

Our programmes

NPMR-047 in candidate selection across two tumour types, with platform expansion planned. Pipeline current as of: 28 July 2026.

Asset	Modality	Biomarker	Indication	Stage	Next milestone
NPMR-047 Lead programme · also known as PDC-1	Synthetic PDC SN-38 payload	Phosphatidylserine (PS)	Colorectal adenocarcinoma; pancreatic ductal adenocarcinoma	Candidate selection	IND/CTA-ready Target: H1 2028
RLT programme Discovery	Targeted radioligand therapy	uPAR	Metastatic colorectal cancer (mCRC)	Discovery	Lead optimisation
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.

View full NPMR-047 asset record ↗

PDC — Peptide Drug Conjugate PS — Phosphatidylserine SN-38 — Active metabolite of Irinotecan (cytotoxic payload) RLT — Radioligand Therapy mCRC — Metastatic Colorectal Cancer uPAR — Urokinase Plasminogen Activator Receptor IND — Investigational New Drug (US FDA) CTA — Clinical Trial Authorisation (UK MHRA)

Data

What the data show

Reproducible findings across colorectal adenocarcinoma and pancreatic ductal adenocarcinoma models from NPMR-047 trials.

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

NPMR-047 has demonstrated superior efficacy to Irinotecan in colorectal adenocarcinoma and pancreatic ductal adenocarcinoma 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.

Mechanism

How NPMR-047 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

NPMR-047 Structure

NPMR-047 is a peptide drug conjugate with three components: a PS-selective binder (orange) that drives tumour accumulation, a proprietary tumour-microenvironment-cleavable linker (blue) that releases the SN-38 anti-cancer payload (black).

NPMR-047 molecule showing orange PS-selective binder, blue tumour-microenvironment-cleavable linker, and black SN-38 payload

Tumour Accumulation & Payload Release

NPMR-047 binds externalised PS on the cancer cell surface and accumulates at the tumour. The timing and the tumour microenvironment then reduce the stability of the linker bond, releasing the SN-38 payload on site.

NPMR-047 binding to externalised phosphatidylserine on the cancer cell membrane and accumulating at the tumour site

Selective Cell Death

Released SN-38 inhibits topoisomerase I, inducing cell death at the tumour site. In preclinical models, NPMR-047 delivered superior tumour growth inhibition at a lower equivalent human dose than Irinotecan, with no treatment-related histopathological changes observed in normal tissues.

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

Dual-Gated Selectivity

Selectivity depends on two conditions being met in sequence. First, NPMR-047 must localise at a site where phosphatidylserine is externalised. Where PS is absent, the molecule clears rapidly from circulation before any payload release can occur. Second, even where the molecule accumulates at off-target sites such as liver or kidney where some PS exposure may occur, the tumour microenvironment is required to trigger linker cleavage. Normal tissue does not provide the same microenvironment as the tumour, so the linker remains stable and the molecule is excreted intact.

Diagram comparing tumour microenvironment where NPMR-047 accumulates and releases payload versus normal tissue and circulation where the molecule is excreted intact

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.

Targeted therapy for patients with no targets.

How we are developing cutting-edge organic chemistry