Myasthenia Gravis Related Research Tools

Myasthenia gravis (MG) is an autoimmune disease caused by antibodies against the acetylcholine receptor (AChR), muscle-specific kinase (MuSK) or other AChR-related proteins in the postsynaptic muscle membrane. Localized or general muscle weakness is the predominant symptom and is induced by the antibodies. Traditionally, most patients with MG require induction therapy with high doses of corticosteroids and maintenance with an immunosuppressant. Nowadays, biologics are emerging as important therapeutic tools that provide better corticosteroid-sparing effects than standard treatments and can even induce remission.

Immunotherapeutics that target different elements in these pathways are shown in yellow boxes. The AChR is presented to CD4+ T cells by antigen-presenting cells (APCs) via co-stimulatory molecules. Downstream upregulation of cytokines stimulates B cells to produce anti-AChR antibodies that lead to the destruction of AChRs by fixing complement at the neuromuscular endplate region. Levels of regulatory T (Treg) and T helper (TH) 17 cells and cytokines are increased in patients with MG, thereby causing the immune imbalance.

Several biologic agents have shown promising effects in studies of their efficacy in MG to date. The success suggests that the emergence of new molecular targets could bring a revolution in the treatment of MG. Creative Biolabs has screened the most popular targets and provides high-quality products as well as customized services for our clients. For more services and products, please contact us.

CD19	CD20	CD80	CD86
IL-2	IL-4	IL-6	IL-17
IL-22	JAK1	JAK2	JAK3
AchR	PD-1	PD-L1	CTLA4
C5	C3	TNF	B cell trophic factor (BAFF)

For Research Use Only. Not For Clinical Use.

Target

CacyBP

ALS2CR1

OPA1

Tenascin C

PGP9.5

GFAP

5-HTR2C

BACE2

POU5F1

Synaptogyrin

Doublecortin

Glypican 1

iNOS

NSE

CDK5

ALS2CR2

NTSR1

CD29

SOD2

NQO1

Mint-1

CDK2

Plexin A2

AHNAK

Pan-KCHIP

NTRK2

NDEL1

NALP

Spastin

STAT3 Phospho (Ser727)

FABP3

Neurofilament L