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<article xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xmlns:ali="http://www.niso.org/schemas/ali/1.0/" article-type="research-article" dtd-version="1.2" xml:lang="en"><front><journal-meta><journal-id journal-id-type="publisher-id">Oncohematology</journal-id><journal-title-group><journal-title xml:lang="en">Oncohematology</journal-title><trans-title-group xml:lang="ru"><trans-title>Онкогематология</trans-title></trans-title-group></journal-title-group><issn publication-format="print">1818-8346</issn><issn publication-format="electronic">2413-4023</issn><publisher><publisher-name xml:lang="en">Publishing House ABV Press</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="publisher-id">1090</article-id><article-id pub-id-type="doi">10.17650/1818-8346-2026-21-1-59-65</article-id><article-categories><subj-group subj-group-type="toc-heading" xml:lang="en"><subject>HEMATOLOGIC MALIGNANCIES: TREATMENT</subject></subj-group><subj-group subj-group-type="toc-heading" xml:lang="ru"><subject>ГЕМОБЛАСТОЗЫ: ЛЕЧЕНИЕ</subject></subj-group><subj-group subj-group-type="article-type"><subject>Research Article</subject></subj-group></article-categories><title-group><article-title xml:lang="en">Mechanism of action of isatuximab in multiple myeloma. Literature review and clinical observation</article-title><trans-title-group xml:lang="ru"><trans-title>Особенности механизма действия изатуксимаба при множественной миеломе. Обзор литературы и клиническое наблюдение</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0003-4142-171X</contrib-id><name-alternatives><name xml:lang="en"><surname>Soloveva</surname><given-names>M. V.</given-names></name><name xml:lang="ru"><surname>Соловьева</surname><given-names>Майя Валерьевна</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><email>solomaiia@yandex.ru</email><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-7944-6202</contrib-id><name-alternatives><name xml:lang="en"><surname>Solovev</surname><given-names>M. V.</given-names></name><name xml:lang="ru"><surname>Соловьев</surname><given-names>М. В.</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><email>solomaiia@yandex.ru</email><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-4966-8146</contrib-id><name-alternatives><name xml:lang="en"><surname>Mendeleeva</surname><given-names>L. P.</given-names></name><name xml:lang="ru"><surname>Менделеева</surname><given-names>Л. П.</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><email>solomaiia@yandex.ru</email><xref ref-type="aff" rid="aff1"/></contrib></contrib-group><aff-alternatives id="aff1"><aff><institution xml:lang="en">National Medical Research Center for Hematology, Ministry of Health of Russia</institution></aff><aff><institution xml:lang="ru">ФГБУ «Национальный медицинский исследовательский центр гематологии» Минздрава России</institution></aff></aff-alternatives><pub-date date-type="pub" iso-8601-date="2026-03-24" publication-format="electronic"><day>24</day><month>03</month><year>2026</year></pub-date><volume>21</volume><issue>1</issue><issue-title xml:lang="en">Oncohematology</issue-title><issue-title xml:lang="ru">Онкогематология</issue-title><fpage>59</fpage><lpage>65</lpage><history><date date-type="received" iso-8601-date="2026-03-09"><day>09</day><month>03</month><year>2026</year></date><date date-type="accepted" iso-8601-date="2026-03-09"><day>09</day><month>03</month><year>2026</year></date></history><permissions><copyright-statement xml:lang="en">Copyright ©; 2026, ABV-press</copyright-statement><copyright-statement xml:lang="ru">Copyright ©; 2026, АБВпресс</copyright-statement><copyright-year>2026</copyright-year><copyright-holder xml:lang="en">ABV-press</copyright-holder><copyright-holder xml:lang="ru">АБВпресс</copyright-holder><license><ali:license_ref xmlns:ali="http://www.niso.org/schemas/ali/1.0/">https://creativecommons.org/licenses/by/4.0/</ali:license_ref></license></permissions><self-uri xlink:href="https://oncohematology.abvpress.ru/ongm/article/view/1090">https://oncohematology.abvpress.ru/ongm/article/view/1090</self-uri><abstract xml:lang="en"><p><bold>Background.</bold> Multiple myeloma (MM) is a malignant lymphoproliferative disorder characterized by tumor plasma cells infiltrating the bone marrow. The pharmaceutical industry for the treatment of MM is experiencing a boom, characterized by the emergence of new-generation targeted drugs. It is important to describe the differences in the binding pattern of monoclonal antibodies to the CD38 protein and to analyze the treatment outcomes of MM patients treated with isatuximab, depending on various biological characteristics of the disease.</p> <p><bold>Aim.</bold> To analyze the literature data on the isatuximab mechanism of action on tumor plasma cells, the features of monoclonal antibodies use depending on various factors and present a clinical observation of the isatuximab therapy in ММ patient and concomitant chronic obstructive pulmonary disease (COPD).</p> <p><bold>Materials and methods.</bold> For this review, PubMed databases, clinical trial registries, and meeting libraries were searched from inception to December 20, 2025, using the terms reflecting multiple myeloma, isatuximab, daratumumab. We analyzed publications devoted to studying the mechanism of action of CD38 monoclonal antibodies and examining the efficacy of isatuximab in the treatment of multiple myeloma, depending on various factors. Our experience with the IsaPd regimen in a patient with relapsed / refractory MM and concomitant COPD is presented.</p> <p><bold>Results.</bold> Isatuximab is the only CD38 antibody capable of inducing direct tumor cell apoptosis. The 1q abnormality did not affect survival in ММ patients treated with isatuximab-containing regimens. Due to limited complement-dependent cytotoxicity, isatuximab may be a preferred option for patients with COPD or asthma. The article describes our experience of isatuximab therapy in MM patient with COPD. The patient was diagnosed with MM in 2015 at the age of 57. Induction therapy consisted of bortezomib- and lenalidomide-containing regimens; an antitumor response was not achieved. Hematopoietic stem cell mobilization was performed after the DHAP regimen (cisplatin, cytarabine, dexamethasone) in combination with granulocyte colony-stimulating factor. To overcome resistance, therapy including carfilzomib was administered, achieving a very good partial remission. Autologous hematopoietic stem cell transplantation (melphalan 200 mg / m<sup>2</sup>) was then performed, followed by local radiation therapy to the plasmacytoma area, resulting in complete remission. Subsequently, due to relapse, therapy including ixazomib and lenalidomide was prescribed. In 2021, due to MM progression, sixth-line anti-relapse therapy with the IsaPd regimen was initiated. Despite COPD with frequent exacerbations requiring bronchodilator therapy, the patient tolerated isatuximab satisfactorily, with no adverse reactions. Twelve courses of therapy were completed, achieving partial remission.</p> <p><bold>Conclusion.</bold> Monoclonal antibodies to CD38 are being integrated into induction therapy protocols for MM patients. This article describes the isatuximab mechanism of action and presents experience using IsaPd as a sixth-line therapy in a patient with MM and COPD. Along with a favorable safety profile, we also observed high treatment efficacy.</p></abstract><trans-abstract xml:lang="ru"><p><bold>Введение.</bold> Множественная миелома (ММ) – злокачественное лимфопролиферативное новообразование, субстратом которого являются опухолевые плазматические клетки, инфильтрирующие костный мозг. Наблюдается подъем индустрии фармакологических средств для лечения ММ, характеризующийся появлением новых поколений препаратов таргетного действия. Представляется важным описать различия способов связывания моноклональных антител с белком CD38 и проанализировать результаты лечения пациентов с ММ, получавших изатуксимаб, в зависимости от различных биологических характеристик заболевания.</p> <p><bold>Цель работы</bold> – проанализировать данные литературы о механизме действия изатуксимаба на опухолевую плазматическую клетку, особенностях применения моноклональных антител в зависимости от различных факторов и представить результаты клинического наблюдения применения изатуксимаба у больной ММ с сопутствующей хронической обструктивной болезнью легких (ХОБЛ).</p> <p><bold>Материалы и методы.</bold> Проведен поиск в базах данных PubMed, реестрах клинических испытаний и библиотеках конференций с момента их создания до 20.12.2025 с использованием терминов «множественная миелома», «изатуксимаб», «даратумумаб». Анализировали публикации, посвященные изучению механизма действия моноклональных антител к белку CD38, исследованию эффективности применения изатуксимаба при лечении ММ в зависимости от различных факторов. Представлен собственный опыт применения схемы IsaРd (изатуксимаб, помалидомид, дексаметазон) у пациентки с рефрактерно-рецидивирующей ММ с сопутствующей ХОБЛ.</p> <p><bold>Результаты.</bold> Изатуксимаб – единственное антитело к CD38, способное вызывать прямой апоптоз опухолевых клеток. Увеличение копийности 1q21 не влияло на показатели выживаемости больных ММ при лечении изатуксимабсодержащими схемами. Ввиду ограниченной комплементзависимой цитотоксичности изатуксимаб может быть предпочтительным вариантом для пациентов с ХОБЛ или астмой. Описан собственный опыт терапии изатуксимабом больной ММ, страдающей ХОБЛ. Диагноз ММ установлен в 2015 г. в возрасте 57 лет. Индукционная терапия проводилась бортезомиб- и леналидомидсодержащими схемами, противоопухолевый ответ не достигнут. Мобилизация гемопоэтических стволовых клеток осуществлена после схемы DHAP (цисплатин, цитозар, дексаметазон) в сочетании с гранулоцитарным колониестимулирующим фактором. Для преодоления резистентности проводили терапию с включением карфилзомиба с достижением очень хорошей частичной ремиссии. Затем выполняли трансплантацию аутологичных гемопоэтических стволовых клеток (мелфалан 200 мг / м<sup>2</sup>) с последующим локальным лучевым воздействием на область плазмоцитомы; констатирована полная ремиссия. Далее в связи с развитием рецидива назначали терапию с включением иксазомиба, леналидомида. В 2021 г. ввиду прогрессирования ММ инициирована противорецидивная терапия 6-й линии по схеме IsaРd. Несмотря на ХОБЛ с частыми обострениями, требующими применения бронходилатирующей терапии, введение изатуксимаба пациентка переносила удовлетворительно, без реакций. Проведено 12 курсов терапии с достижением частичной ремиссии.</p> <p><bold>Заключение.</bold> В протоколы индукционной терапии больных ММ интегрируются моноклональные антитела к CD38. В настоящей статье описаны особенности механизма действия изатуксимаба и представлен опыт применения IsaРd в качестве 6-й линии терапии у больной ММ, страдающей ХОБЛ. При благоприятном профиле безопасности наблюдается высокая эффективность проводимой терапии.</p></trans-abstract><kwd-group xml:lang="en"><kwd>multiple myeloma</kwd><kwd>isatuximab</kwd><kwd>monoclonal antibody to CD38</kwd><kwd>extramedullary disease</kwd><kwd>chromosome 1q21 amplification</kwd><kwd>chronic obstructive pulmonary disease</kwd></kwd-group><kwd-group xml:lang="ru"><kwd>множественная миелома</kwd><kwd>изатуксимаб</kwd><kwd>моноклональное антитело к CD38</kwd><kwd>экстрамедуллярное поражение</kwd><kwd>амплификация 1q21</kwd><kwd>хроническая обструктивная болезнь легких</kwd></kwd-group><funding-group/></article-meta></front><body></body><back><ref-list><ref id="B1"><label>1.</label><mixed-citation>Padala S.A., Barsouk A., Barsouk A. et al. Staging, and management of multiple myeloma. Med Sci (Basel) 2021;9(1):3. DOI: 10.3390/medsci9010003</mixed-citation></ref><ref id="B2"><label>2.</label><mixed-citation>Dimopoulos M.A., Moreau P., Terpos E. et al. 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