gMG, yea you know me
gMG Path
gMG MOAs
NMOSD
NMOSD MOAs
100

This number of gMG cases have detectable levels of anti-AChR antibodies, which activate complement

What is 85%

100

Anti-AChR Antibodies trigger activation of complement through this pathway

What is the classical pathway?

100

These therapies work by binding and depleting
B cells, thereby preventing B-cell activation and proliferation

What are B cell inhibitors?

100

This percentage of patients may not fully recover from their first NMOSD clinical event

What is 76%

100

These work by inhibiting terminal complement and preventing formation of the MAC and astrocyte damage

What are complement inhibitors?
200

The MOST SENSITIVE test for AChR and MuSK autoantibodies

What is cell-based assay (CBA)?

200

This leads to membrane destruction
over time

What is Complement Activation?

200

These therapies inhibit terminal complement and prevent formation of the MAC at the NMJ

What are complement inhibitors?

200

The female to male ratio in NMOSD

What is 5:1?

200

These therapies work by binding and depleting
B cells, thereby preventing B-cell activation and proliferation

What are B-cell inhibitors?

300

The most troublesome symptom reported by patients

What is fatigue?

300

A decreased number or function of these impacts muscle control in patients with gMG

What is AChRs?

300

This blocks FcRn receptor and reduces circulating IgG levels

What are FcRn inhibitors?

300

NMOSD in patients of this ancestry is characterized by earlier onset, increased severity of relapses, and increased mortality

What is African ancestry?

300

This therapy leads to T-cell inactivation, B-cell and autoantibody reduction

What is IVIG?

400

This percentage of patients with ocular symptoms progress to generalized symptoms

What is 75%?

400

The reduced function or number of AChRs causes a reduction in  this, resulting in impaired muscle contraction

What is EPP generation?

400

This therapy works by T-cell inactivation, B-cell and autoantibody reduction

What is IVIG?

400

The primary site of damage in NMOSD

What are astrocytes?

400

These therapies work to inhibit enzymes to reduce protein synthesis or action at lymphocytes

What are immunosuppressants?
500

This leads to depolarization of
the muscle membrane and muscle contraction

What is binding of ACh to AChR?

500

 In gMG, these cells secrete
anti-AChR antibodies that target the NMJ

What are plasma cells?

500

These therapies interfere with cellular synthesis, replication, and proliferation; inhibiting interleukin synthesis

What are immunosuppressants?

500

In patients with NMOSD, these
bind to AQP4 and initiate formation of lesions via complement activation

What are anti-AQP4 antibodies?

500

These therapies work to reduce plasmablast survival, AQP4 antibody production, BBB deterioration, and pathogenic Th17 cell differentiation

What are IL-6 inhibitors?

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