Advanced Research Services

Synovo's own drug discovery programs across inflammation, oncology, and age-related disease

Synovo's research work runs alongside our preclinical services. Founded in 2004 and grown to roughly 40 scientists across three sites in Tübingen, we pursue our own drug discovery programs in parallel with partner-funded research.

Synovo has built sixteen patent families and a peer-reviewed publication record spanning inflammation, oncology, CNS, age-related diseases, antimicrobials, and vaccines. The three programs below are illustrative examples; the underlying platforms — lysosomal targeting, macrolide-conjugate chemistry, and translational disease models — extend across the broader portfolio.

SELECTED PUBLICATIONS

Retinal degeneration

Clearing lipofuscin from the retinal pigment epithelium

Lipofuscin accumulation in the RPE drives age-related macular degeneration and Stargardt disease. Synovo's pharmacokinetic and tissue-distribution work supported the discovery that soraprazan, renamed Remofuscin, removes existing lipofuscin from the RPE — a mechanism long thought impossible. A single intravitreal injection rescues retinal function in a mouse model of advanced Stargardt disease.

Selected publications

Julien-Schraermeyer, S. et al. Penetration, distribution, and elimination of remofuscin/soraprazan in Stargardt mouse eyes following a single intravitreal injection using pharmacokinetics and transmission electron microscopic autoradiography: Implication for the local treatment of Stargardt’s disease and dry age-related macular degeneration. Pharmacology Research & Perspectives 8, e00683 (2020).

Fang, Y. et al. Removal of RPE lipofuscin results in rescue from retinal degeneration in a mouse model of advanced Stargardt disease: Role of reactive oxygen species. Free Radical Biology and Medicine 182, 132–149 (2022).

Removal of lipofuscin in primary human RPE cells after treatment with Remofuscin (Fang et al. 2022)

Immune-cell targeting

Delivering anti-inflammatories into immune-cell lysosomes

Conjugating drug payloads to azalide macrolide carriers traps them in the lysosomes of immune cells, where many inflammatory pathways originate. Applied to fumaric esters, the lysosomal 2'-ester of monomethyl fumarate proved roughly 300-fold more potent than DMF in a psoriasis model, supporting GPR109A as the in vivo target. The same lysosomal-trapping platform underpins our defined-diet EAE model for multiple sclerosis.

Selected publications

Straß, S. et al. Immune cell targeted fumaric esters support a role of GPR109A as a primary target of monomethyl fumarate in vivo. Inflammopharmacol 31, 1223–1239 (2023).

Martorelli, M. et al. A Defined Diet Combined with Sonicated Inoculum Provides a High Incidence, Moderate Severity Form of Experimental Autoimmune Encephalomyelitis (EAE). ACS Pharmacol. Transl. Sci. 7, 3827–3845 (2024).

BALB/c mice (n = 8) treated with imiquimod cream for 7 days, dosed daily with compounds 1–3, DMF, or vehicle. Skin score, body weight, and AUC shown.

Autoimmune disease

Selective JAK3 inhibitors that preserve IL-10 signaling

JAK3 is expressed almost exclusively in leukocytes. Selective inhibition suppresses TNFα and IL-6 while leaving IL-10 signaling intact, producing a more favorable cytokine profile than pan-JAK inhibitors. Our covalent-reversible JAK3 inhibitors, coupled to macrolide carriers, concentrate in immune cells and barrier epithelia and raise the IL-10/TNFα ratio at low systemic doses.

Selected publications

Laux, J. et al. Selective Inhibitors of Janus Kinase 3 Modify Responses to Lipopolysaccharides by Increasing the Interleukin-10-to-Tumor Necrosis Factor α Ratio. ACS Pharmacol. Transl. Sci. 6, 892–906 (2023).

Laux, J. et al. Inherent Fluorescence Demonstrates Immunotropic Properties for Novel Janus Kinase 3 Inhibitors. ACS Pharmacol. Transl. Sci. 6, 1433–1452 (2023).