Elotuzumab in the treatment of relapsed and refractory multiple myeloma

2021 ◽  
Author(s):  
Sebastian Grosicki ◽  
Martyna Bednarczyk ◽  
Agnieszka Barchnicka ◽  
Olga Grosicka
Keyword(s):  
Multiple Myeloma ◽  
Monoclonal Antibodies ◽  
Natural Killer Cells ◽  
Natural Killer ◽  
Clinical Studies ◽  
Mechanisms Of Action ◽  
Incurable Disease ◽  
The Us ◽  
Us Fda ◽  
Humanized Monoclonal Antibodies

Multiple myeloma (MM) is still considered an incurable disease. However, drugs with different mechanisms of action that can improve the efficiency of treatment offer hope. Still, there are concerns about an unacceptable increase in toxicity with such regimens. The results of recently published clinical studies of elotuzumab in combination with lenalidomide/dexamethasone or pomalidomide/dexamethasone confirm previous hopes to improve the effect of that treatment. Humanized monoclonal antibodies aimed at SLAMF7 stimulate natural killer cells to fight against MM cells. Elotuzumab used in combination with lenalidomide/dexamethasone or with pomalidomide/dexamethasone is approved by the US FDA to treat patients with relapsed and/or refractory MM. The article is a summary of the recent knowledge about the possibility of using elotuzumab in the treatment of relapsed and/or refractory MM and shows its potential uses in the future.

Treatment with humanized monoclonal antibodies against CD80 and CD86 combined with sirolimus prolongs renal allograft survival in cynomolgus monkeys1

2003 ◽  
Vol 75 (12) ◽  
pp. 2106-2113 ◽  
Author(s):  
Tudor B??rsan ◽  
Bernard Hausen ◽  
John P. Higgins ◽  
Richard W. Hubble ◽  
Jochen Klupp ◽  
...  
Keyword(s):  
Monoclonal Antibodies ◽  
Renal Allograft ◽  
Allograft Survival ◽  
Humanized Monoclonal Antibodies

scholarly journals Anti-CGRP monoclonal antibodies: a breakthrough in the treatment of migraine

2019 ◽  
Vol 9 (5) ◽  
pp. 262-267
Author(s):  
Julia Azimova ◽  
Yaroslav Ashikhmin ◽  
Mikhail Kukushkin ◽  
Aleksandr Amelin ◽  
Kirill Skorobogatykh
Keyword(s):  
Monoclonal Antibodies ◽  
Adverse Effects ◽  
Adverse Reactions ◽  
Prophylactic Treatment ◽  
Botulinum Toxin A ◽  
Beta Blockers ◽  
Episodic Migraine ◽  
New Class ◽  
Humanized Monoclonal Antibodies ◽  
Severe Adverse Reactions

To date, the prophylactic treatment of migraine has included only nonspecific drugs of various pharmacological groups: the beta-blockers propranolol and metoprolol, the anticonvulsants topiramate and valproic acid, the antidepressants amitriptyline and venlafaxine, candesartan, and Ona botulinum toxin A. As these drugs were developed for treatment of other diseases, their use was associated with adverse effects: decreased blood pressure, mental retardation, weight increase, nausea, and some others. CGRP is a neuropeptide that was regarded as the main biomarker of migraine as its level in this disease rise. The emergence of humanized monoclonal antibodies has opened up the possibility of blocking the action of CGRP and developing a new class of drugs that includes fremanezumab, erenumab, galcanezumab, and eptinezumab. Anti-CGRP monoclonal antibodies can be prescribed to patients with chronic and episodic migraine. The use of anti-CGRP monoclonal antibodies in clinical studies was associated with a small number of adverse effects, with severe adverse reactions being extremely rare.

Paraneoplastic disorders and neuroimmunology

2011 ◽  
Author(s):  
Neil Scolding
Keyword(s):  
Monoclonal Antibodies ◽  
B Cell ◽  
Neurological Disorders ◽  
Therapeutic Potential ◽  
Immune Therapy ◽  
Clinical Consequences ◽  
Humanized Monoclonal Antibodies

The extraordinary expansion in the field of neuroimmunology witnessed in the last decade is not just in the number of neurological disorders now considered to have an immune basis, nor the depth of understanding of disorders long known to be ‘neuroimmune’. Nor is it in the number of antibodies discovered and now testable, nor in the range of new immune suppressant or modifying treatments now emerging or already available. It is of course all of these things, but it is also more than the sum of these parts. What we are currently privileged to witness is the coming together of immunological understanding, the neurobiology of disease, and rational immune therapy, or at least the beginning of this process. To take one isolated example, neurogenetics and neurophysiology taught us about the clinical consequences of channel disruption; laboratory-based neuroimmunology showed antibodies to be capable of producing comparable acquired disease; and it seems likely that specific anti-B-cell humanized monoclonal antibodies offer the therapeutic potential to remove these channel-disrupting antibodies. Neither of these steps could be described in the last edition, and one can imagine similar dramatic changes will emerge before the next.

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