Pancreatic beta cells restoration mass and function diabetes cure
Pancreatic beta cells mass and function restoration as a diabetes cure.

Diabetes Cure

Restore insulin making beta cells using Menin-MLL Disruptor.

2013 – 2019

Our origin

Developing a small molecule to restore insulin secreting functional beta cells mass to cure Type 2 Diabetes (T2D). T2D is a subset of metabolic disease disorders. Molecular mechanism of a small molecule ~500 Dalton that interrupts menin-MLL interaction in a nutshell below.

Disrupts a specific interaction, blocking Menin and MLL

Target protein Menin binds to many other proteins

Menin interruption increases insulin producing beta cells

Identify small molecule with high affinity to disrupt


In the year 2025, a brief summary on other companies’ menin inhibitors: [2, 4, 6]

Several companies are currently working on menin inhibitors, including Syndax Pharmaceuticals (with Revumenib), Kura (with Ziftomenib), Sumitomo Pharma, Daiichi Sankyo, Biomea Fusion, Janssen (Johnson & Johnson), and Easton. [1, 2, 3, 4, 5, 6]

Syndax Pharmaceuticals: Developed Revumenib, the first FDA-approved menin inhibitor. [2, 4, 6]   With acute leukemia, the abnormal leukemia cells multiply very quickly and take over the space in the bone marrow. This blocks the cells from turning into normal healthy blood cells. Acute lyphoid leukemia (or ALL) and acute myeloid leukemia (or AML) are two different types of acute leukemia that stop cells from developing into healthy blood cells and lower your healthy blood cell count. When first diagnosed with ALL or AML, a workup of tests are completed to identify the exact type of acute leukemia a patient has. Part of that workup includes genetic testing that can detect the genetic changes, such as mutations and gene rearrangements, that may have caused a specific type of ALL or AML. Rearrangements of the MLL / KMT2A gene (KMT2A-r) cause approximately 10% of acute leukemias.1 It is estimated that more than 95% of patients with KMT2A-r acute leukemia have a MLL-r / KMT2A translocation, a type of rearrangement that occurs when part of one chromosome breaks and fuses to a different chromosome.2

Kura: Developing Ziftomenib, another prominent menin inhibitor in clinical trials. [1, 3, 6] Most cancer drugs work by killing diseased cells faster than they kill healthy tissue. But what if you didn’t have to kill the cancer cell? What if you could convince it to become a healthy cell? That’s the mechanism underlying an emerging class of targeted therapies called menin inhibitors.  Menin interating MLL KMT2A or MLLr – KMT2Ar

Sumitomo Pharma: Working on DSP-5336, a menin inhibitor in early clinical phases. [1, 3, 5]  Sumitomo Dainippon Pharma will continue to develop the compound as an anti-cancer drug, aiming to apply for the patients with the acute myeloid leukemia with MLL gene rearrangements or with NPM1 mutations.

Daiichi Sankyo: Developing DS-1594b, a menin inhibitor currently in clinical trials. [3, 4, 7]

Biomea Fusion: Investigating BMF-219, a menin inhibitor in early clinical stages. [1, 3, 4]  Clinical trial 2a for diabetes treatment in Sept 2025.

Reference Cited
[1] https://www.nature.com/articles/d41573-024-00106-3
[2] https://pmc.ncbi.nlm.nih.gov/articles/PMC10881917/
[3] https://www.clinicaltrialsarena.com/analyst-comment/aml-menin-inhibitors/
[4] https://finance.yahoo.com/news/global-menin-inhibitor-drugs-clinical-094800101.html
[5] https://www.vjhemonc.com/video/current-data-on-menin-inhibition-in-aml/
[6] https://www.nature.com/articles/d41573-024-00198-x
[7] https://journals.lww.com/journalppo/fulltext/2022/01000/menin_inhibitors_in_acute_myeloid_leukemia_what.9.aspx