Pipeline

MRM-XRT

Radiation therapy (XRT ) is mainstay treatment for local prostate cancer, 45% of patients choose XRT as first line treatment.

However, current problems include:

Injury to healthy cells/ tissues – Side effects
High doses of radiation required
Limited efficacy – Ultimately leading to recurrence

MRM-XRT is a triple advantage approach to radiation sensitization:

MRM-XRT actively targets cancer cells and not healthy cells
Gold nanoparticle core enhances radiation due to photoelectric effect
MRM-XRT molecularly enhances radiation damage by increasing cellular oxidation

MRM-XRT will enable lower XRT doses, limit side effects, and increase cancer cell eradication rates. No drug exists that sensitizes cells to XRT and increases damage via targeted reduction of GPX4.

Initial indication is radiation resistant prostate cancer with expansion to other types.

MRM-ON1

MRM-ON1 is a novel approach for targeting solid tumors through the cell-surface receptor SR-B1 to regulate lipid metabolism. MRM-ON1 binds to SR-B1 to inhibit cellular cholesterol uptake, a dependent nutrient for cancer cells, while also turning on a downstream metabolic cellular cascade that down regulates the antioxidant enzyme glutathione peroxidase 4 (GPX4). GPX4 is a gatekeeper of oxidative damage in tumor cells, and down regulation leads to increased oxidative stress that ultimately kills the cancer cells.

Solid Tumor indications include:

Platinum resistant ovarian
Prostate
Kidney
Pancreas

The company has completed its pre-IND meeting and is preparing for final enabling toxicity studies.

MRM-ON1

A large amount of preclinical data support MRM-ON1 therapy for many hematological cancers. Several hematological cancers express SR-B1 and similarly to solid tumors, these cancers are highly sensitive to cholesterol depletion and disruption of lipid metabolism by downregulation of GPX4. Ultimately, like solid tumors MRM-ON1 therapy results in potent cell killing.

Hematological indications include:

Acute Myeloid Leukemia (AML)
Diffuse Large B-cell Lymphoma (DLBCL)
Follicular Lymphoma
Chronic Lymphocytic Leukemia (CLL)

MRM-CV1

Atherosclerotic cardiovascular disease (ASCVD) is a disease of non-functional high-density lipoproteins (HDL). Individuals with CVD lack sufficient amounts of functional HDL to support the protective properties HDLs provide. HDLs are unique structures that have several protective functions that aid in preventing CVD. HDLs sequester and transport cholesterol to the liver for excretion, reduce inflammation at the site of atherosclerotic lesions, and maintain endothelia integrity and repair through antioxidative and antithrombotic properties. MRM-CV1 has been engineered to mimic the natural protective functions of native HDL resulting in the reversal of and prevention of CVD.

Protective functions of HDLs:

Reverse cholesterol transport
Cholesterol efflux capacity
Vasodilatory activity
Antithrombotic activity
Antioxidant activity
Anti-inflammatory activity

MRM-CV1 replaces non-functional HDLs to inhibit and reverse CVD:

Enhances cholesterol efflux
Reduces inflammation
Increases antioxidant activity
Eliminates plaque formation

Heart disease remains the most common cause of death in the world. Current treatments for cardiovascular disease leave unaddressed residual disease. MRM-CV1 directly addresses the root causes of CVD. MRM-CV1 address the failures of past treatment modalities, by being the first and only mature spherical mimic of native HDL. This breakthrough in engineering stems from building an HDL mimic using an organic scaffold, whereupon the targeting protein apolipoprotein A-I assembles with the scaffold and enables the self-assembly of HDL lipids. MRM-CV1 engages with the receptor SR-B1 to remove cholesterol and provide anti-inflammatory and antioxidant signaling. Due to the unique spherical nature, MRM-CV1 has shown profound reduction of plaque formation in the arterial wall in preclinical disease models.

Phase I clinical trial for MRM-CV1 begins recruitment in 2026.

MRM-OT1

HDL plays a critical role in maintaining corneal epithelial cell homeostasis and reduces inflammation. SR-B1, the HDL receptor, is expressed by corneal epithelial cells, limbal epithelia cells, stromal epithelial cells, and stromal keratocytes. In preclinical corneal wound models, including in diabetic models, topical application of MRM-OT1 significantly enhanced wound closure. Additional studies found MRM-OT1 to attenuate initial stages of inflammation resulting from chemical burns and other cell stressors. Overall, data suggest MRMs can be developed to treat acute and chronic inflammatory eye conditions, like dry eye, atopic keratoconjunctivitis, bacterial keratitis, eye injuries from chemical or thermal injury, long-term contact lens wear, and post-surgical treatment to enhance wound healing.