Intracerebral haemorrhage (ICH) is the second-most common form of stroke. Due to the post-ICH brain damage and limited therapeutic strategies, the disability rate among ICH survivors is high. DJ-1 is a protein known to play roles in cytoprotection. However, DJ-1 can be oxidised and lose its protective functions. Our study investigated the oxidation state of DJ-1 after ICH and the therapeutic potential of DJ-1 oxidation inhibitor, DJ-1-binding compound 23 (Comp-23), in ICH. We induced experimental ICH mice models by intra-striatal injection of collagenase. Immunoblot, qPCR measurement and immunohistochemistry showed that while DJ-1 expression was not significantly changed, oxidised DJ-1 was dramatically increased in the perihematomal region after ICH. A similar trend was observed in the hemin-induced ICH in-vitro model. We evaluated the sensorimotor functions after ICH using three behavioural tests, including the Modified Neurological Severity Score, Rotarod Accelerating Test and Grid Walking Test. ICH mice treated with Comp-23 performed better in these tests within the first week post-ICH compared to ICH mice treated with vehicle. Luxol fast blue staining, transmission electron microscopy, and Fluoro-Jade C staining showed reduced post-ICH demyelination and neuronal death in the treatment group, possibly contributing to its better post-ICH sensorimotor performance. Cell viability assay, Liperfluo staining, and FerroOrange staining in the ICH in-vitro model showed that Comp-23 significantly reduced neuronal death and cell lipid peroxidation. Overall, our data suggested that anti-DJ-1-oxidation can reduce neurofunctional deficits after ICH and tends to exert neuroprotective effects related to anti-ferroptosis.