VAT N° 01537970525
What we do
UCme BIOSCIENCE
is a Siena (Italy) company developing innovative therapeutic antibody candidates that have the potential to revolutionize the treatment of patients with Age-Related Macular Degeneration (AMD) and cancer worldwide.
Aged-Related Macular Degeneration
Age-related macular degeneration (AMD) is a chronic, progressive and severe disease of the central retina (“macula”). The neovascular (“wet”) form of the disease is the most common cause of irreversible vision loss in developed countries and is due to abnormal vessel growth in the choroid and/or retina. In 2021, there were a total of approximately 20 million diagnosed cases of wet AMD worldwide. The prevalence of AMD increases steadily with age. As the world population ages, the number of people with wet AMD will also increase.
A LEADING CAUSE OF IRREVERSIBLE BLINDNESS AND VISUAL IMPAIRMENT
20 MILLION DIAGNOSED CASES OF WET AMD WORLDWIDE
PREVALENCE EXPECTED TO INCREASE BY 50% BY 2040
AMD treatment
Although the use of monoclonal antibodies against vascular endothelial growth factor (VEGF) has revolutionized the treatment of neovascular AMD, the long-term results of anti-VEGF therapy are poor in half of the patients treated. The persistence of choroidal neovascularization (CNV) despite VEGF blockade and the recurrence of neovascular growth and leakage during treatment breaks leave significant needs.
MANY PATIENTS DO NOT RESPOND OPTIMALLY
FREQUENT AND INDEFINITE EVALUATIONS REQUIRED
SHORT DURATION EFFECT
LOSS OF RESPONSE OVER TIME
What we do
With the aim of obtaining new tools to inhibit blood vessel growth in AMD and tumors, we generated a library of monoclonal antibodies (mAbs) against surface molecules of endothelial cells (ECs). Because ECs have a different antigen profile during active angiogenesis than quiescent cells in stable vessels, we immunized mice with proliferating human ECs (HUVEC) to obtain mAbs that can block the function of proteins involved in the angiogenic process. Among the mAbs obtained, we isolated an antibody that recognizes human CD93 with high affinity and has been shown to be suitable for targeting angiogenesis in choroid and tumors.
CD93 as a new target for AMD treatment
CD93 is a transmembrane protein that is predominantly and highly expressed in neovascular membranes of AMD patients and in tumor endothelial cells, and several data suggest that CD93 plays an important role in angiogenesis both as a soluble growth factor and as an adhesion molecule. Because CD93 has been identified as an important regulator of angiogenesis, it represents a potential new target for hyperproliferative ECs in choroidal neovascular (CNV) membranes and developing tumors.
CD93 is strongly expressed in endothelial cells of CNV membranes from AMD patients and tumor blood vessels and weakly expressed in nonproliferating endothelium. It is also noteworthy that ablation of CD93 impedes choroidal angiogenesis. Much evidence suggests that CD93 mediates adhesion in endothelium, and we identified multimerin 2 (MMRN2), an extracellular matrix protein, as a specific ligand for CD93. We found that CD93 and MMRN2 are co-expressed in the blood vessels of various human tumors and CNV membranes. Importantly, the anti-CD93 antibody we are developing counteracts angiogenesis by blocking this interaction.
In October 2023 we obtained the approval of the
Italian Patent Application
(N. 102021000021764) for our anti-CD93 antibody.
Development in cancer therapy
Angiogenesis plays a critical role in the growth of cancer because solid tumors require a blood supply if they are to grow beyond a size of a few millimeters. Tumors can actually cause this blood supply by sending chemical signals that stimulate angiogenesis. Tumors can also stimulate nearby normal cells to produce angiogenesis signaling molecules.
The resulting new blood vessels supply growing tumors with oxygen and nutrients, allowing the tumor to enlarge and the cancer cells to invade nearby tissues, spread throughout the body, and form new colonies of cancer cells called metastases.
Because tumors cannot grow beyond a certain size or spread without a blood supply, we plan to develop our anti-CD93 antibody as a tumor angiogenesis inhibitor as well.
Following our initial research, interest in targeting CD93 to treat cancer is growing rapidly: Recently, it has been demonstrated that high vascular CD93 expression correlates with poor survival in human gliomas, that increased expression of CD93 promotes angiogenesis and tumor growth in nasopharyngeal carcinomas, that blockade of the CD93 pathway normalizes tumor vasculature to facilitate drug delivery and immunotherapy, and that a polymorphism of the CD93 gene is associated with disseminated colorectal cancer.
