The safety and efficacy of the agents and/or uses under investigation have not been established. There is no guarantee that the agents will receive health authority approval or become commercially available in any country for the uses being investigated.
Proposed Mechanism of Action
Ozanimod is an oral, sphingosine-1-phosphate (S1P) receptor modulator that binds with high affinity selectively to S1P subtypes 1 (S1P1) and 5 (S1P5).1 Because both S1P1 and S1P5 are expressed on multiple cells throughout the body, including the central nervous system (CNS), they represent a target for ozanimod that can potentially lead to clinically relevant neuroprotection.1-4 Ozanimod can modulate S1P1 expression, resulting in the retention of autoreactive T and B cells in lymphoid tissue and decreasing their circulation in the blood stream. A reduction in these types of lymphocytes prevents their migration to sites of inflammation.1,5 Preclinical studies demonstrated a reversible reduction in circulation of B and T lymphocytes in multiple sclerosis (MS) animal models.6
Ozanimod Propose Mechanism of Action

Ozanimod, an S1P1 and S1P5 modulator is hypothesized to prevent S1P-mediated lymphocyte migration from lymphoid organs to the CNS 1, 5, 6
ozanimod by Disease State
ozanimod in Multiple Sclerosis
Phase 3
Relapsing Multiple Sclerosis
View Trials Investigating ozanimod in Multiple Sclerosis
View Rationale for Clinical Development
Rationale for Clinical Development
The blood-brain barrier prevents peripheral immune cells from entry into the CNS; however, in MS, the blood-brain barrier is disrupted, allowing infiltration of these cells. Autoreactive T and B cells in the CNS contribute to chronic inflammatory processes that result in myelin and axonal damage7-10 The sphingosine-1-phosphate (S1P) pathway is hypothesized to play an important role in the chronic inflammation associated with MS.11,12 Ozanimod selectively targets S1P1 and S1P5 receptors, which are expressed on multiple cells throughout the CNS.3,4 In MS, ozanimod is thought to retain autoreactive T and B cells in lymphoid tissue, thus preventing their migration into the CNS.1,5 Hence, S1P receptor modulation reduces the number of circulating T and B lymphocytes, and potentially decreases the damage caused by these cells when they infiltrate the blood-brain barrier.
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