Our science
Our program connects published metabolic research with a formulation strategy and the studies needed to evaluate it.
01 / Biological rationale
Many cancers use fatty-acid synthesis to support growth. Their dependence varies, and they can also obtain lipids from their surroundings.
One-minute science film / Optional music
How ACC connects lipid synthesis, fatty-acid oxidation, and a therapeutic hypothesis in cancer.
The studies shown provide scientific rationale. They do not establish clinical benefit or the performance of NMG’s formulation. Improved therapeutic index remains our development goal.
Acetyl-CoA carboxylase, or ACC, converts acetyl-CoA into malonyl-CoA. The film distinguishes two isoforms: ACC1 supplies malonyl-CoA for fatty-acid synthesis in the cytosol; ACC2 produces malonyl-CoA near mitochondria, where it inhibits CPT1 and limits fatty-acid oxidation. A dual inhibitor acts on both ACC1 and ACC2.
The film presents published preclinical research in lung cancer and endocrine-resistant breast cancer, alongside work reporting that ACC inhibition induces endoplasmic reticulum stress and enhances anticancer drug activity in preclinical models. These findings provide scientific rationale; they are not evidence of NMG formulation performance.
The film also introduces PF-05175157, a dual ACC1/ACC2 inhibitor developed by Pfizer and studied in people. Platelet-making cells also depend on fatty-acid synthesis, creating a development challenge for systemic ACC inhibition. The film describes the platelet effect as dose-dependent and reversible.
NMG’s objective is to concentrate ACC inhibition in tumors while limiting exposure elsewhere. This remains a development objective, not a demonstrated result, and the lead breast cancer program is preclinical.
ACC1 uses ATP and bicarbonate to convert acetyl-CoA to malonyl-CoA. Fatty acid synthase uses acetyl-CoA, malonyl-CoA, and NADPH to produce palmitate, which feeds downstream lipid metabolism. ACC2 also regulates fatty-acid oxidation.
Published preclinical studies support investigating ACC inhibition in cancer. NMG’s goal is a formulation with improved therapeutic index. Tumor dependencies vary, and clinical benefit remains to be established.
Sources: ACC1 reaction, fatty acid synthesis, Marczyk et al., 2022, and Shan et al., 2026.
02 / Delivery rationale
Published studies in healthy participants found dose-dependent reductions in platelet counts with a systemically distributed ACC inhibitor. Drug exposure and tolerability are therefore central questions for formulation development.
Our objective is to change how the drug is delivered. Improved tumor exposure and reduced healthy-tissue exposure remain benefits to test.
Read the platelet biology study03 / Treatment design
Targeting identifies a binding partner. The delivered drug determines which cellular mechanism is engaged.
In a retrospective study, Mai and colleagues examined sequential treatment with Trodelvy and Enhertu in metastatic breast cancer. These medicines target different proteins but carry payloads from the same drug class.
Separately, Rampa and colleagues found that switching to microtubule-inhibiting ADC payloads restored activity in particular resistant breast-cancer models. This preclinical work supports investigating drug mechanism alongside targeting.
The question for NMG
The ADC studies provide broader treatment-design context. Neither tested ACC inhibition or NMG’s formulation, or established that our approach overcomes ADC resistance.
See how we are approaching the question04 / The lead formulation
An ACC-inhibitor formulation using biodegradable polymer nanoparticles, with TROP2-directed targeting planned for evaluation.
TROP2 / Planned evaluation
We plan to evaluate a TROP2-directed ligand as part of formulation development. Binding, uptake, and the benefit of adding a ligand each require experimental validation.
TROP2 is also expressed in normal tissues. Its presence on cancer cells alone does not establish tumor-selective delivery.
TROP2 expression in human tissues
Particle characteristics, drug loading, release, stability, and batch consistency inform candidate selection. Targeting is an additional property that requires its own validation.
Development prioritiesSelected research
Shan et al. / Clinical Cancer Research / 2026
Shan and colleagues’ 2026 study, with senior author Lajos Pusztai, examines ACC inhibition, cellular stress, and combinations with other cancer therapies.
Explore the 2026 studyMarczyk et al. / Cancer Research / 2022
Marczyk and colleagues’ metabolic analysis provides a foundation for selecting ACC as a therapeutic target.
Explore the foundational study