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<p>Tarlatamab, a bispecific T-cell engager (BiTE), effectively activates the immune system but often causes cytokine release syndrome (CRS). To understand the early in vivo cytokine dynamics of post-BiTE therapy, we analyzed serum from three SCLC patients before and after tarlatamab administration using the Bio-Plex Pro Human Cytokine Screening Panel, 48-Plex. CRS occurred once in case 1, twice in case 2, and not at all in case 3. During the initial CRS in cases 1 and 2, IL-6, IL-1Ra, IL-10, granulocyte colony-stimulating factor, MIG, and IP-10 increased from baseline. Of these, MIG and IP-10 were also elevated during the second CRS episode in case 2. Some cytokines (hepatocyte growth factor, IFN-α2, IFN-γ, IL-2Rα, MIP-1α, MCP-1, and TRAIL) rose during CRS in either case 1 or 2 but showed little change in the other. RANTES decreased during CRS in case 1, yet increased and remained high in case 2, and stayed elevated in case 3. This cytokine profiling highlights the complex pathophysiology of CRS and the involvement of diverse cytokine networks beyond the IL-6 axis. These findings may guide future biomarker development, disease classification, and therapeutic strategies beyond IL-6 inhibition, advancing personalized CRS management.</p>

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Early trajectory of inflammatory cytokines following tarlatamab administration in three advanced SCLC patients

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月21日

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  • Takuma Imakita,
  • Kohei Fujita,
  • Yuki Yamamoto,
  • Osamu Kanai,
  • Yuta Okada,
  • Shogo Toyama,
  • Takanori Ito,
  • Issei Oi,
  • Kiminobu Tanizawa

摘要

Tarlatamab, a bispecific T-cell engager (BiTE), effectively activates the immune system but often causes cytokine release syndrome (CRS). To understand the early in vivo cytokine dynamics of post-BiTE therapy, we analyzed serum from three SCLC patients before and after tarlatamab administration using the Bio-Plex Pro Human Cytokine Screening Panel, 48-Plex. CRS occurred once in case 1, twice in case 2, and not at all in case 3. During the initial CRS in cases 1 and 2, IL-6, IL-1Ra, IL-10, granulocyte colony-stimulating factor, MIG, and IP-10 increased from baseline. Of these, MIG and IP-10 were also elevated during the second CRS episode in case 2. Some cytokines (hepatocyte growth factor, IFN-α2, IFN-γ, IL-2Rα, MIP-1α, MCP-1, and TRAIL) rose during CRS in either case 1 or 2 but showed little change in the other. RANTES decreased during CRS in case 1, yet increased and remained high in case 2, and stayed elevated in case 3. This cytokine profiling highlights the complex pathophysiology of CRS and the involvement of diverse cytokine networks beyond the IL-6 axis. These findings may guide future biomarker development, disease classification, and therapeutic strategies beyond IL-6 inhibition, advancing personalized CRS management.