KOL Call Highlights Beta Cell Restoration for Type 1 Diabetes: BMEA, CRSP, IPSC

Research evidence excerpt

KOL Call Highlights Beta Cell Restoration for Type 1 Diabetes: BMEA, CRSP, IPSC

is to maintain partnerships. These companies may invest more

glucose levels within a healthy range over time. In T1D, the beta cells are destroyed by than budgeted and require additional funding

autoimmune cell attack. Immune inhibitors like Tzield (teplizumab) can help delay the from the capital markets. These companies

progression of Stage 2 to Stage 3 T1D by deactivating T cells and increasing Tregs to could face future unforeseen litigation.

protect beta cells from attack. However, T1D patients are heterogenous with involvement

of different immune pathways and cells types accounting for lack of response in some

patients and waning of response over time. Ultimately, the KOL thinks the combination

of immune therapies with mechanisms that increase the beta cell mass could provide

greater benefit. Likewise, GLP-1 therapies have helped in T1D, but some patients are

resistant and others discontinue due to side effects. The KOL indicated that combining

GLP-1s with therapies that increase beta cell proliferation is an important next step that

could reap the benefits of GLP-1 at lower doses to improve tolerability. Finally, it has been

established that allogeneic beta cell transplant can be curative, but the KOL highlighted

the required life-long immunosuppression as a major limitation.

• Menin Inhibition Increases Beta Cell Proliferation. Biomea's (BMEA, Tenthoff)

icovamenib is an oral covalent menin inhibitor. The KOL explained that menin is a tumor

suppressor and inhibitor of beta cell proliferation. During pregnancy, menin is naturally

inhibited by prolactin and placental lactogen, allowing the mother to produce more beta