Nipocalimab
(Synonyms: M281) 目录号 : GC68301Nipocalimab (M281) 是一种全人源的重组非糖基化 IgG1 单克隆抗体。Nipocalimab 是一种人去糖基化 IgG1 抗 FcRn 单克隆抗体，在体内 pH 6.0 和胞外 pH 7.6 下均以皮摩尔亲和力与Fc 受体 (FcRn) 结合。
Cas No.:2211985-36-1
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Nipocalimab (M281) is a fully human, recombinant, aglycosylated IgG1 monoclonal antibody. Nipocalimab is a human deglycosylated IgG1 anti-FcRn monoclonal antibody that binds with picomolar affinity to Fc receptor (FcRn) at both endosomal pH 6.0 and extracellular pH 7.6[1][2].
[1]. James S Castleman, et al. Medical therapy to attenuate fetal anaemia in severe maternal red cell alloimmunisation. Br J Haematol. 2021 Feb;192(3):425-432.
[2]. Marinos C Dalakas, et al. The importance of FcRn in neuro-immunotherapies: From IgG catabolism, FCGRT gene polymorphisms, IVIg dosing and efficiency to specific FcRn inhibitors. Ther Adv Neurol Disord. 2021 Feb 26;14:1756286421997381.
| Cas No. | 2211985-36-1 | SDF | Download SDF |
| 别名 | M281 | ||
| 分子式 | 分子量 | ||
| 溶解度 | 储存条件 | Store at -20°C | |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Pharmacotherapy of Generalized Myasthenia Gravis with Special Emphasis on Newer Biologicals
Drugs 2022 Jun;82(8):865-887.PMID:35639288DOI:10.1007/s40265-022-01726-y.
Myasthenia gravis (MG) is a chronic, fluctuating, antibody-mediated autoimmune disorder directed against the post-synaptic neuromuscular junctions of skeletal muscles, resulting in a wide spectrum of manifestations ranging from mild to potentially fatal. Given its unique natural course, designing an ideal trial design for MG has been wrought with difficulties and evidence in favour of several of the conventional agents is weak as per current standards. Despite this, acetylcholinesterases and corticosteroids have remained the cornerstones of treatment for several decades with intravenous immunoglobulins (IVIG) and therapeutic plasma exchange (PLEX) offering rapid treatment response, especially in crises. However, the treatment of MG entails long-term immunosuppression and conventional agents are viable options but take longer to act and have a number of class-specific adverse effects. Advances in immunology, translational medicine and drug development have seen the emergence of several newer biological agents which offer selective, target-specific immunotherapy with fewer side effects and rapid onset of action. Eculizumab is one of the newer agents that belong to the class of complement inhibitors and has been approved for the treatment of refractory general MG. Zilucoplan and ravulizumab are other agents in this group in clinical trials. Neisseria meningitis is a concern with all complement inhibitors, mandating vaccination. Neonatal Fc receptor (FcRn) inhibitors prevent immunoglobulin recycling and cause rapid reduction in antibody levels. Efgartigimod is an FcRn inhibitor recently approved for MG treatment, and rozanolixizumab, Nipocalimab and batoclimab are other agents in clinical trial development. Although lacking high quality evidence from randomized clinical trials, clinical experience with the use of anti-CD20 rituximab has led to its use in refractory MG. Among novel targets, interleukin 6 (IL6) inhibitors such as satralizumab are promising and currently undergoing evaluation. Cutting-edge therapies include genetically modifying T cells to recognise chimeric antigen receptors (CAR) and chimeric autoantibody receptors (CAAR). These may offer sustained and long-term remissions, but are still in very early stages of evaluation. Hematopoietic stem cell transplantation (HSCT) allows immune resetting and offers sustained remission, but the induction regimens often involve serious systemic toxicity. While MG treatment is moving beyond conventional agents towards target-specific biologicals, lack of knowledge as to the initiation, maintenance, switching, tapering and long-term safety profile necessitates further research. These concerns and the high financial burden of novel agents may hamper widespread clinical use in the near future.
Medical therapy to attenuate fetal anaemia in severe maternal red cell alloimmunisation
Br J Haematol 2021 Feb;192(3):425-432.PMID:32794242DOI:10.1111/bjh.17041.
Haemolytic disease of the fetus and newborn (HDFN) remains an important cause of fetal mortality with potential neonatal and longer-term morbidity. HDFN is caused by maternal red cell alloimmunisation, with IgG antibodies crossing the placenta to destroy fetal erythroid cells expressing the involved antigen. Intrauterine fetal blood transfusion is the therapy of choice for severe fetal anaemia. Despite a strong evidence base and technical advances, invasive fetal therapy carries risk of miscarriage and preterm birth. Procedure-related risks are increased when invasive, in utero transfusion is instituted prior to 22 weeks to treat severe early-onset fetal anaemia. This review focuses upon this cohort of HDFN and discusses intravenous immunoglobin (IVIg) and novel monoclonal antibody (M281, Nipocalimab) treatments which, if started at the end of the first trimester, may attenuate the transplacental passage and fetal effects of IgG antibodies. Such therapy has the ability to improve fetal survival in this severe presentation of HDFN when early in utero transfusion may be required and may have wider implications for the perinatal management in general.
New Therapies for the Treatment of Warm Autoimmune Hemolytic Anemia
Transfus Med Rev 2022 Oct;36(4):175-180.PMID:36182620DOI:10.1016/j.tmrv.2022.08.001.
In this review article we provide a critical insight into recent reports evaluating innovative therapies for warm type autoimmune hemolytic anemia (wAIHA). Among published articles, we selected two reports on the use of the proteasome inhibitor bortezomib in association with dexamethasone or rituximab, one study on the spleen tyrosine kinase inhibitor fostamatinib, and a retrospective study on recombinant erythropoietin (rEPO). Among recent scientific communications, we discussed a report on the phosphoinositide 3-kinase delta inhibitor (PI3Kδi) parsaclisib. All studies highlighted a good efficacy although to be confirmed in larger trials and with limitations due to the heterogeneity of wAIHA patients enrolled, the small number of subjects, the concomitant medications allowed, and the short follow-up. Ongoing trials include new B-cell/plasma-cell targeting agents such as the Bruton tyrosine kinase inhibitors ibrutinib and rilzabrutinib, and the anti-CD38 MoAbs daratumumab and its analogue isatuximab. Further drugs in clinical trials target the complement cascade in wAIHA with complement activation, such as the C3 inhibitor pegcetacoplan and the C1q inhibitor ANX005. Finally, an interesting and non-immuno-toxic strategy is to remove the pathogenic autoantibodies via blocking the neonatal Fc receptor, by intravenous Nipocalimab and subcutaneous RVT-1401. Such novel agents targeting the several immunopathological mechanisms acting in wAIHA and their possible combination, will increase the therapeutic armamentarium and possibly fill the gap of wAIHA relapsed after/refractory to rituximab. Moreover, these new target therapies may represent a tool for the unmet need of very acute cases.
The importance of FcRn in neuro-immunotherapies: From IgG catabolism, FCGRT gene polymorphisms, IVIg dosing and efficiency to specific FcRn inhibitors
Ther Adv Neurol Disord 2021 Feb 26;14:1756286421997381.PMID:33717213DOI:10.1177/1756286421997381.
The neonatal Fc receptor (FcRn) binds endogenous IgG and protects it from lysosomal degradation by transporting it back to the cell surface to re-enter the circulation, extending the serum IgG life span. FcRn plays a role in the function of IVIg because the supraphysiological IgG levels derived from IVIg administrations saturate the FcRn allowing the endogenous IgG to be degraded, instead of being recycled, resulting in high levels of infused IgG ensuring IVIg efficiency. New data in myasthenia gravis patients suggest that the that the Variable Number of Tandem 3/2 (VNTR3/2) polymorphisms in FCGRT, the gene that encodes FcRn, may affect the duration of infused IgG in the circulation and IVIg effectiveness. This review addresses these implications in the context of whether the FCGRT genotype, by affecting the half-life of IVIg, may also play a role in up to 30% of patients with autoimmune neurological diseases, such as Guillain-Barré syndrome, CIDP or Multifocal Motor Neuropathy, who did not respond to IVIg in controlled trials. The concern is of practical significance because in such patient subsets super-high IVIg doses may be needed to achieve high IgG levels and ensure efficacy. Whether FCGRT polymorphisms affect the efficacy of other therapeutic monoclonal antibodies by influencing their distribution clearance and pharmacokinetics, explaining their variable effectiveness, is also addressed. Finally, the very promising effect of monoclonal antibodies that inhibit FcRn, such as efgartigimod, rozanolixizumab and Nipocalimab, in treating antibody-mediated neurological diseases is discussed along with their efficacy in the IgG4 subclass of pathogenic antibodies and their role in the blood-brain barrier endothelium, that abundantly expresses FcRn.