Company: GLPG
Filing Date: 2025-03-27
Form Type: 20-F
Source: 0001558370-25-003806
Chunk: 114

Company: GALAPAGOS NV
Filing Date: 2025-03-27
Form: 20-F
Item: Item 4
Chunk 114
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 to Alfasigma, the revenues and costs related to Jyseleca® for the full years 2024, 2023 and 2022, are presented separately from the results of the Company’s continuing operations on the line ‘Net profit from discontinued operations, net of tax’ in the consolidated income statement.
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Under the terms of the agreement, Galapagos received a €50 million upfront payment and is eligible to receive potential sales-based milestone payments totaling €120 million and mid-single to mid-double-digit earn-outs on European sales. Galapagos will contribute up to €40 million to Alfasigma by June 2025 for Jyseleca® related development activities.
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  2.    TYK2 program: GLPG3667
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<{self.tag} alt="{self.alt}" src="{self.src}"><{self.tag} alt="{self.alt}" src="{self.src}">We are advancing our TYK2 inhibitor, GLPG3667, in two Phase 3-enabling studies for systemic lupus erythematosus (SLE) and dermatomyositis (DM). Patient randomization of the SLE study was completed in February 2025, ahead of schedule. Topline results for the entire GLPG3667 program are anticipated in the first half of 2026.
Following the planned strategic reorganization as announced early this year, we are seeking potential partners to take over our small molecule assets, including GLPG3667 for SLE, DM, and other potential auto-immune indications.
GLPG3667 is an investigational reversible and selective TYK2 kinase domain inhibitor that was discovered by us and evaluated in a Phase 1 healthy volunteer study in 2020. The Phase 1 study was a randomized, double-blind, placebo-controlled dose escalation study evaluating safety, tolerability, pharmacokinetics (PK) and pharmacodynamics (PD) of single and multiple ascending oral doses of GLPG3667 for 13 days.
Blood was drawn at multiple time points on Day 1 and on Day 10 and stimulated ex vivo with several cytokines, including IFNα, to analyze the level of inhibition of inflammation, including the effect on phosphorylated signal transducer and activator of transcription (pSTAT) signaling as well as hematological parameters, lipids, and creatine phosphokinase (CPK) (see graphs below).

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Following these results, we initiated a randomized, placebo-controlled, double