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市場調查報告書
商品編碼
1636799
2025 年全球 CD39 標靶治療臨床試驗、治療方法與市場機會Global CD39 Targeted Therapies Clinical Trials, Therapeutic Approaches & Market Opportunity Insight 2025 |
CD39 標靶治療已成為調節多種疾病免疫反應的一種有前途的策略。CD39 作為影響嘌呤訊號通路的關鍵外核甘酸酶,從而調節免疫活化和抑制之間的平衡。CD39 透過將 ATP 轉化為 AMP,然後透過 CD73 進一步轉化為腺甘,從而幫助建立免疫抑制微環境。這種環境對腫瘤特別有利,但在慢性感染和自體免疫疾病中也發揮作用。阻斷 CD39 活性可能會恢復免疫功能並改善這些情況下患者的預後。
在腫瘤學中,CD39 對腫瘤微環境 (TME) 中的免疫抑制的貢獻已得到充分證實。腫瘤常利用 CD39-CD73-腺甘軸來逃避免疫監視,導致免疫細胞耗竭和抗腫瘤反應受損。調節性 T 細胞 (Treg) 和 CD8+ T 細胞上 CD39 水平升高與多種惡性腫瘤預後不良有關。使用針對 CD39 的單株抗體(例如 IPH5201),可以重新激發免疫系統,更有效地對抗腫瘤細胞。IPH5201 由 Innate Pharma 和阿斯特捷利康共同開發,目前正在研究與免疫檢查點抑制劑 (ICI) 聯合使用以增強實體瘤患者的免疫反應。
除了癌症之外,CD39 標靶療法也可能用於其他疾病,特別是慢性病毒感染、自體免疫疾病和敗血症。在愛滋病毒、結核病和恰加斯病等慢性傳染病中,CD39 參與免疫衰竭和抑制,阻止有效的免疫反應。阻斷CD39可能逆轉免疫功能障礙並提高人體消除病原體的能力。在免疫系統過度活躍的自體免疫疾病中,針對 CD39 可能有助於重新平衡調節性 T 細胞的抑制功能,這對於防止組織損傷至關重要。
由於單核細胞和巨噬細胞上的 CD39 表現對於控制發炎非常重要,因此針對 CD39 的治療潛力也延伸至敗血症。在敗血症中,實現平衡的免疫反應對於有效控制感染同時減少組織損傷至關重要。透過抑制 CD39 活性,治療幹預可以抑制過度發炎並恢復免疫穩態,代表了對抗這種嚴重病理的新策略。
CD39 標靶治療的臨床進展仍處於早期階段,其中有幾種候選藥物正在進行臨床試驗,特別是第 2 期試驗。其中,IPH5201脫穎而出,成為領先的候選藥物,在臨床前和早期臨床試驗中均顯示出良好的結果。這些抗體不僅在腫瘤學領域進行評估,而且在 CD39 在免疫調節中發揮重要作用的各種慢性疾病中進行評估。透過聚焦 CD39,這些療法旨在增強免疫抑製或功能障礙情況下的免疫反應。
未來,針對CD39的治療的潛在應用前景十分深遠。將抗 CD39 抗體與其他療法(例如免疫檢查點抑制劑或抗病毒藥物)結合,可以產生協同效應並提供增強免疫反應的機會。然而,課題依然存在,特別是關於 CD39 在不同疾病和患者群體中的環境相關功能。實現免疫活化和抑制之間的精確平衡對於安全有效地實施這些療法至關重要。隨著臨床試驗的進展和更多數據的收集,CD39 標靶療法可能成為個人化醫療的基本組成部分,從而實現精確和可控的免疫反應,有效治療各種疾病。
本報告研究了全球 CD39 標靶治療市場,並概述了市場以及藥物趨勢、臨床試驗趨勢、區域趨勢以及參與市場的公司的競爭格局。
Global CD39 Targeted Therapies Clinical Trials, Therapeutic Approaches & Market Opportunity Insight 2025 Report Highlights:
CD39 targeting therapies are emerging as a promising strategy for modulating immune responses in a range of diseases. CD39 serves as a vital ectonucleotidase that influences the purinergic signaling pathway, thereby regulating the equilibrium between immune activation and suppression. By converting ATP into AMP, which is further transformed into adenosine by CD73, CD39 is instrumental in establishing an immunosuppressive microenvironment. This environment is particularly advantageous for tumors but also plays a role in chronic infections and autoimmune diseases. Inhibiting CD39 activity may restore immune functionality and enhance patient outcomes in these contexts.
In the realm of oncology, the contribution of CD39 to immune suppression within the tumor microenvironment (TME) is well-established. Tumors frequently utilize the CD39-CD73-adenosine axis to evade immune surveillance, resulting in immune cell exhaustion and diminished anti-tumor responses. Elevated levels of CD39 on regulatory T cells (Tregs) and CD8+ T cells have been associated with unfavorable prognoses in various malignancies. By employing monoclonal antibodies that target CD39, such as IPH5201, it is possible to reactivate the immune system to more effectively combat tumor cells. IPH5201, which is being developed by Innate Pharma and AstraZeneca, is currently under investigation in conjunction with immune checkpoint inhibitors (ICIs) to enhance the immune response in patients with solid tumors.
In addition to cancer, CD39-targeting therapies show considerable potential for addressing other diseases, particularly chronic viral infections, autoimmune disorders, and sepsis. In the context of chronic infections like HIV, tuberculosis, and Chagas disease, CD39 is implicated in immune exhaustion and suppression, which obstructs effective immune responses. By inhibiting CD39, there is a possibility of reversing immune dysfunction and improving the body's capacity to eliminate pathogens. In autoimmune disorders, where there is an overactivation of the immune system, the targeting of CD39 may aid in reestablishing equilibrium by enhancing the inhibitory function of regulatory T cells, which are vital for averting tissue damage.
The therapeutic promise of targeting CD39 also encompasses sepsis, as CD39 expression on monocytes and macrophages is instrumental in regulating inflammation. In the context of sepsis, achieving a balanced immune response is crucial to mitigate tissue injury while effectively managing infection. By inhibiting the activity of CD39, therapeutic interventions could diminish excessive inflammation and restore immune homeostasis, presenting a novel strategy for addressing this critical condition.
The clinical advancement of therapies aimed at CD39 is still in its nascent phase, with several candidates progressing through clinical trials, particularly in Phase 2. Among these, IPH5201 stands out as a leading candidate, demonstrating encouraging outcomes in both preclinical and early-phase clinical investigations. These antibodies are being assessed not only in oncology but also across a range of chronic conditions where CD39 plays a significant role in immune regulation. By focusing on CD39, these therapies seek to bolster immune responses in scenarios characterized by immune suppression or dysfunction.
Looking forward, the potential uses of CD39-targeting therapies are extensive. The integration of anti-CD39 antibodies with other treatment modalities, such as immune checkpoint inhibitors or antiviral therapies, presents the opportunity for synergistic effects, thereby enhancing the immune response. Nonetheless, challenges persist, particularly concerning the context-dependent function of CD39 across various diseases and patient demographics. Achieving a precise balance between immune activation and suppression will be essential for the safe and effective implementation of these therapies. As clinical trials advance and additional data is collected, therapies targeting CD39 may emerge as a fundamental component of personalized medicine, effectively addressing various diseases through the precise and controlled modulation of immune responses.
Figure 2 -1: CD39 Inhibition - Mechanism