Sanofi halts riliprubart MOBILIZE phase 3 study in patients with chronic inflammatory demyelinating polyneuropathy

10 June 2026

Sanofi announced that the riliprubart MOBILIZE phase 3 study in patients with chronic inflammatory demyelinating polyneuropathy (CIDP), refractory to standard-of-care treatment, will be stopped. This disappointing outcome follows Phase 2 trials that had shown promising results, with 87% of standard-of-care patients improving or remaining stable after switching to riliprubart.

Riliprubart was previously granted orphan drug designation in the EU, US and Japan for treating CIDP.

The decision to halt MOBILIZE phase 3 study was motivated by an independent data monitoring committee’s analysis of interim data, which determined that the MOBILIZE study was unlikely to provide sufficient efficacy. No safety signals related to riliprubart were identified as part of this analysis. The press release also mentioned that Sanofi was still assessing whether to continue the other global phase 3 trial - VITALIZE - which is comparing riliprubart to intravenous immunoglobulin in patients who responded to the standard-of-care.

Riliprubart is a humanized monoclonal antibody targeting complement C1s. Its efficacy was established in Hesperos' Human-on-a-Chip model of CIDP using co-cultures of human iPSC-derived motoneurons and primary Schwann cells. Adding serum from CIDP patients to the platform triggered auto-antibody binding, classical complement activation, and electrophysiological deficits.

By testing the ability of riliprubart to rescue electrophysiological deficits in a CIDP-on-a-chip, Hesperos had demonstrated mechanistic plausibility that C1s inhibition could rescue complement‑mediated neuromuscular dysfunction, providing supportive preclinical data that helped Sanofi advance the drug into clinical trials.

The reasons for which the phase 3 trial did not mirror the success of the phase 2 are unknown and will undoubtedly be analyzed by the drugmaker.

Generally speaking, while complementing animal models with new approach methodologies/non-animal models is often presented as a way to “bridge the translational gap,” the reality is more sober: stacking preclinical models does not automatically produce more predictive science. In this particular case, we could not find a publication or a Sanofi press release that would have indicated that the drugmaker also relied on findings in animal models of CIDP, such as for example

Experimental Autoimmune Neuritis (EAN) rodent models.

In itself, the Hesperos platform is a valuable tool for mechanistic proof-of-concept and IND support. While it accurately captured complement-driven acute effects, CIDP-on-a-chip may have overestimated how well isolated C1s inhibition would perform in treatment-refractory chronic CIDP where additional pathomechanisms may dominate.

It is entirely possible that the CIDP-on-a-chip model was deliberately reductionist: focused on acute humoral/complement-mediated effects but not on cellular immunity, full nerve microenvironment or other chronic processes. The phase 3 trials may have brought to light unknown clinical heterogeneity in CIDP, whether in phenotype, immune drivers or etiology.

In order to make informed decisions about future research directions, Sanofi plans to analyze in detail the data from this MOBILIZE study. 

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