Memento brings home $93M series A souvenir, picks up bispecific for eye diseases

Memento Secures $93M Series A, Licenses Bispecific for Eye Diseases

Memento Medicines has successfully raised $93 million in Series A funding to advance its newly licensed lead asset, MMT-205, a bispecific antibody targeting retinal disorders. The Boston-based biotech secured worldwide rights to MMT-205 from MabTics and Curacle through an exclusive deal involving upfront cash and equity. MMT-205 is designed to block the VEGF pathway and activate the Tie2 receptor simultaneously, aiming to improve upon current monotherapies for conditions like neovascular age-related macular degeneration (nAMD) and diabetic macular edema (DME). The funding will support investigational new drug (IND)-enabling studies, expected to begin next year.

• Memento Medicines announced a successful $93 million Series A funding round, co-led by Forbion, RA Capital Management, and Avego BioScience Capital, with additional participation from Sanofi Ventures and Samsara BioCapital. This significant investment will fuel the development of its new lead program, MMT-205, for retinal disorders.
• In conjunction with the funding, Memento secured an exclusive worldwide licensing deal for MMT-205 from MabTics and Curacle. The agreement includes unspecified upfront cash and equity payments, along with potential future R&D, regulatory, and commercial milestone payments, as well as tiered royalties on net sales if the molecule reaches the market.
• MMT-205 is a novel bispecific antibody engineered to simultaneously block the VEGF pathway and activate the Tie2 receptor. This dual mechanism is intended to enhance the integrity of blood vessels in the retina, offering a potentially best-in-class biologic therapy for conditions such as neovascular age-related macular degeneration (nAMD) and diabetic macular edema (DME), with IND-enabling studies planned for next year.

Overcoming Current Limitations in nAMD and DME Treatment

Current anti-VEGF therapies for neovascular AMD (nAMD) have meaningfully reduced the incidence of severe vision loss, yet substantial clinical and operational gaps persist. Achieving durable, vision-restoring outcomes across the full patient population remains an unmet need, driven by biological, mechanistic, and real-world treatment delivery challenges.

• Suboptimal visual outcomes in real-world practice: More than half of patients exhibit inadequate or null responses to VEGF-A–targeting agents such as ranibizumab. Despite the demonstrated efficacy of ranibizumab, aflibercept, and bevacizumab in reducing severe visual impairment, patients typically experience some degree of vision loss over time. Current treatment goals are largely oriented toward visual stabilisation rather than vision restoration, and in patients who continue to decline despite therapy, the functional and quality-of-life consequences can be profound.

• High treatment burden from frequent intravitreal injections: Repeated intravitreal injections impose significant burden on both patients and healthcare systems. Conventional approaches do not prevent disease recurrence, necessitating ongoing retreatment with no clear endpoint, which affects adherence and long-term outcomes.

• Incomplete understanding of disease pathogenesis: Treatment success has historically been constrained by an incomplete characterisation of nAMD mechanisms. Conventional strategies were developed under the assumption that the angiogenic switch is governed solely by classical angiogenic growth factors; however, other VEGF family members — including VEGF-C and VEGF-D, which activate VEGFR-2 and VEGFR-3 — have also been implicated in disease pathogenesis. This mechanistic complexity likely underlies the heterogeneous treatment responses observed with VEGF-A–selective agents.

• Evidence and data gaps for key agents: Reliable safety and efficacy data for bevacizumab remain unavailable in this indication, and no robust data exist for combination therapies. Additionally, phase III results for pegaptanib and ranibizumab are not directly comparable, particularly with respect to outcomes observed in control groups, limiting cross-trial inference.

• Absence of personalised and biomarker-driven treatment frameworks: The course of therapy may require rapid modification in certain patients based on individual response profiles. Furthermore, a differentiated, evidence-based framework for interpreting retinal fluid by OCT compartment — as a marker of disease activity — has not been fully established, complicating treat-and-extend or PRN decision-making.

• Inadequate guidance on treatment switching: Criteria for switching to alternative treatment modalities are not well-standardised, despite clinical consensus that switching should be considered when first-line therapy proves ineffective.

Dual-Targeting: A New Frontier in Retinal Disease

The landscape of retinal disease treatment, particularly for neovascular age-related macular degeneration (nAMD) and diabetic macular edema (DME), has been revolutionized by anti-vascular endothelial growth factor (anti-VEGF) therapies. However, despite their effectiveness, these treatments come with significant limitations. Patients often require frequent intravitreal injections, leading to a substantial burden on individuals and healthcare systems. Moreover, a notable proportion of patients experience suboptimal visual outcomes, and long-term anti-VEGF therapy has been associated with complications like macular atrophy.

Memento Medicines' recent funding round and licensing of MMT-205 signal a strategic pivot towards addressing these persistent challenges. MMT-205's bispecific mechanism, which simultaneously inhibits the VEGF pathway and activates the Tie2 receptor, represents a promising next-generation approach. This dual-targeting strategy aims to enhance both the efficacy and durability of treatment, potentially reducing the need for frequent injections and improving long-term patient outcomes. The literature suggests that multifaceted approaches are often necessary when single-pathway blockades prove insufficient, and targeting the Tie2 pathway in combination with VEGF inhibition is an area of active research.

However, the path forward is not without its hurdles. As an early-stage asset, MMT-205 faces the inherent risks of clinical development, where many promising therapies do not ultimately reach patients. The safety profile of a novel bispecific mechanism will require careful scrutiny, particularly given the long-term nature of treatment for these chronic conditions and the known side effects of existing therapies. Furthermore, MMT-205 will enter a highly competitive market already populated by several established anti-VEGF agents and a robust pipeline of other innovative therapies, including long-acting formulations, sustained-release implants, and gene therapies. To succeed, MMT-205 will need to demonstrate clear, superior clinical benefits that justify its adoption over existing and emerging options, ultimately offering a more convenient and effective solution for patients.