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| Primary information |
|---|
| ID | 15781 |
| Therapeutic ID | Th1627 |
| Protein Name | Efgartigimod alfa |
| Sequence | >Th1627_Efgartigimod_alfa
DKTHTCPPCPAPELLGGPSVFLFPPKPKDTLYITREPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALKFHYTQKSLSLSPGK
|
| Molecular Weight | 54000 |
| Chemical Formula | NA |
| Isoelectric Point | NA |
| Hydrophobicity | NA |
| Melting point | NA |
| Half-life | The terminal elimination half-life of efgartigimod alfa ranges from 80 to 120 hours.[L39496] |
| Description | Myasthenia gravis (MG) is an autoimmune disorder characterized by significant muscle weakness - particularly in the eye, throat, and extremities - caused by autoantibodies attacking the neuromuscular junction.[A243759] The production of IgG autoantibodies against acetylcholine receptors (AChRs) is one of the more common pathophysiological mechanisms behind MG, and results in the destruction of these receptors and a reduction in electrical nerve impulses.[A243759] Efgartigimod alfa is a first-in-class[L39501] antagonist of the neonatal Fc receptor (FcRn) used in the treatment of myasthenia gravis (MG).[L39496] IgG antibodies, including the autoantibodies responsible for MG symptoms, can be 'recycled', a process which significantly extends their half-life, by evading lysosomal degradation via binding with FcRn.[L39509] By antagonizing this interaction, efgartimod alfa prevents this recycling phase and thus decreases the half-life of IgG, effectively lowering circulating levels of IgG autoantibodies against AChRs. Efgartimod alfa was granted FDA approval on December 17, 2021.[L39501] |
| Indication/Disease | Efgartigimod alfa is indicated for the treatment of generalized myasthenia gravis in adult patients who are anti-acetylcholine receptor antibody-positive.[L39496] |
| Pharmacodynamics | Efgartigimod alfa exerts its pharmacologic effect by reducing circulating levels of the autoantibody responsible for myasthenia gravis symptoms. It is administered as a once-weekly intravenous infusion, given for 4 weeks per treatment cycle, with the option to initiate additional treatment cycles as clinically indicated after at least 50 days have passed following the previous cycle.[L39496] Because efgartigimod alfa reduces circulating IgG levels, patients undergoing therapy may be at greater risk of infection due to a depressed immune response.[L39496] It should not be initiated in patients with an active infection, and consideration should be given to holding therapy in patients who develop a serious infection during a treatment cycle. |
| Mechanism of Action | Myasthenia gravis (MG) is an autoimmune disorder affecting the neuromuscular junction of the skeletal muscles.[A243759] While the pathophysiologic mechanisms of MG differ depending on the subtype in question, all forms involve the production of IgG autoantibodies to some endogenous protein. One of the most commonly implicated proteins against which autoantibodies are produced are acetylcholine receptors (AChRs), which undergo degradation via the membrane attack complex (MAC) secondary to their interaction with AChR-specific autoantibodies.[A243759] The destruction of AChRs prevents regular transmission of electrical impulses across the neuromuscular junction, which ultimately leads to the characteristic muscular weakness - especially of the eyes, throat, and extremities - observed in patients with MG. Immunoglobulin G, as opposed to other immunoglobulins, undergoes a recycling phase in the vascular endothelium that dramatically extends its half-life.[L39509] In the case of pathogenic IgGs causing MG, this may facilitate an increased ability to impair neuromuscular transmission. This recycling involves IgG binding to the neonatal Fc receptor (FcRn), which rescues IgG from lysosomal degradation.[L39509] Efgartigimod alfa is a human IgG1 antibody fragment that binds to FcRn, thus preventing IgG recycling and subsequently reducing the amount of circulating IgG, including the autoantibodies responsible for MG.[L39496,L39509] |
| Toxicity | There are no data regarding overdosage with efgartigimod alfa. |
| Metabolism | As with other therapeutic proteins, efgartigimod alfa is likely metabolized to smaller peptides and amino acids via proteolytic enzymes.[L39496] |
| Absorption | NA |
| The volume of distribution of efgartigimod alfa ranges from 15 to 20 liters.[L39496] |
| Clearance | NA |
| Categories | Human Immunoglobulin G |
| Patents Number | NA |
| Date of Issue | NA |
| Date of Expiry | NA |
| Drug Interaction | NA |
| Target | IgG receptor FcRn large subunit p51 |
| Brand Name | Vyvgart |
| Company | argenx US |
| Brand Description | argenx US |
| Prescribed For | Intravenous |
| Chemical Name | 20 mg/1mL |
| Formulation | None. |
| Physical Appearance | respiratory tract infections, headache, urinary tract infection (UTI), numbness and tingling, and muscle pain. |
| Route of Administration | Vyvgart is used in adults to treat myasthenia gravis. Vyvgart may also be used for purposes not listed in this medication guide. |
| Recommended Dosage | Vyvgart is a prescription medicine used to treat the symptoms of Myasthenia gravis (gMG) in adults who test positive for the antiacetylcholine receptor (AChR) antibody. Vyvgart may be used alone or with other medications. |
| Contraindication | NA |
| Side Effects | NA |
| Useful Link 1 | Link |
| Useful Link 2 | Link |
| Remarks | NA |