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🧠 Disease-Modifying Therapy Mechanism Simulator

A comparison of the mechanisms of action for ocrelizumab (anti-CD20), natalizumab (anti-α4-integrin), and fingolimod (S1P receptor modulator) with visualization of their impact on lymphocyte migration across the blood-brain barrier.

Multiple Sclerosis2DModerate60 FPS
ms-dmt-mechanism-comparison-simulator ↗ Open standalone

Unchecked Lymphocyte Trafficking Across the Blood-Brain Barrier

Placeholder: autoreactive lymphocytes cross the BBB and attack myelin.

  • 100%: CNS infiltration (baseline) (relative, no therapy)
  • 100: Circulating lymphocytes (relative baseline units)
  • ~0.4–0.6: Annual relapse rate (untreated) (placeholder reference)
  • high: Myelin attack events (placeholder qualitative)

Why lymphocytes reach the CNS

Placeholder: activation, adhesion, transmigration steps summarized briefly.

Consequence of unchecked infiltration

Placeholder: demyelination and relapse risk without intervention.

Three Drug Classes, Three Distinct Points of Intervention

Placeholder: pick ocrelizumab, natalizumab, or fingolimod to compare.

  • CD20: Ocrelizumab target (B-lymphocyte surface marker)
  • α4-integrin: Natalizumab target (adhesion receptor)
  • S1P1: Fingolimod target (sphingosine-1-phosphate receptor)
  • IV / IV / oral: Route (placeholder dosing summary)

Depletion vs. blockade vs. retention

Placeholder: each drug intercepts the attack at a different stage.

Choosing between mechanisms

Placeholder: efficacy, risk, and monitoring trade-offs briefly noted.

How Each Therapy Physically Interrupts the Attack

Placeholder: antibody depletion, integrin blockade, or lymph-node trapping.

  • B-cell depletion: Ocrelizumab action (anti-CD20 antibody binding)
  • Adhesion blockade: Natalizumab action (α4-integrin / VCAM-1 blocked)
  • Lymph node retention: Fingolimod action (S1P1 internalization traps cells)
  • weeks–months: Onset of action (placeholder timeframe)

Ocrelizumab — anti-CD20 depletion

Placeholder: antibody binds CD20, marks B-cells for clearance.

Natalizumab — integrin blockade

Placeholder: blocks adhesion so cells cannot cross the BBB wall.

Fingolimod — S1P receptor modulation

Placeholder: lymphocytes stay sequestered inside lymph nodes.

CNS Infiltration Falls as Each Mechanism Takes Hold

Placeholder: three routes converge on the same outcome — quieter CNS.

  • ~82%: Ocrelizumab infiltration cut (placeholder max effect)
  • ~96%: Natalizumab infiltration cut (placeholder max effect)
  • ~78%: Fingolimod infiltration cut (placeholder max effect)
  • ~6–12 mo: Time to plateau (placeholder curve shape)

Infiltration curves over therapy duration

Placeholder: effect builds over months, not instantly.

Myelin attack quiets accordingly

Placeholder: fewer lymphocytes in CNS, fewer attack events.

Relapse Reduction Achieved, at Different Monitoring Costs

Placeholder: comparable efficacy, divergent safety monitoring needs.

  • ~47%: Ocrelizumab relapse reduction (placeholder trial figure)
  • ~68%: Natalizumab relapse reduction (placeholder trial figure)
  • ~54%: Fingolimod relapse reduction (placeholder trial figure)
  • varies: Key risks (infection / PML / cardiac-ocular)

Efficacy compared across mechanisms

Placeholder: natalizumab highest, ocrelizumab and fingolimod close behind.

Distinct side-effect and monitoring profiles

Placeholder: infusion/infection, PML, or cardiac/ocular monitoring.

Drug-specific monitoring at a glance

ProductIndicationTrial DesignKey Result
Ocrelizumab
Natalizumab
Fingolimod
⚙ Under the hood

A comparison of the mechanisms of action for ocrelizumab (anti-CD20), natalizumab (anti-α4-integrin), and fingolimod (S1P receptor modulator) with visualization of their impact on lymphocyte migration across the blood-brain barrier.

CanvasBiomedicine

2D · HTML5 Canvas 2D · 60 FPS target · runs fully client-side, no install

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