若生智能
Drug Database
T-

T-Bactum (EB23 18235Y / EB2318235Y)

✓ Approved

Essex Bio-Technology Limited · 治疗药物

什么是 T-Bactum？

T-Bactum 是一种治疗药物，由Essex Bio-Technology Limited研发。该药已获批，用于治疗相关适应症，给药途径：Oral (PO)。

药物档案

商品名EB23 18235Y, EB2318235Y
公司Essex Bio-Technology Limited
给药途径Oral (PO)
状态Approved
来源： ClinicalTrials.gov, Essex Bio-Technology Limited

治疗适应症

T-Bactum 针对 1 个适应症，涉及 1 个治疗领域。

治疗领域疾病/病症分期
Infections and infestationsOral infection✓ Approved

相关研究文献

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Feng Shi S, Kong Ran R, Xiao Li L, Zhou Xiangxiang X

Dual-target chimeric antigen receptor T (CAR-T) cell therapy has emerged as a promising strategy to address the key limitations of single-target CAR-T approaches, including antigen heterogeneity and antigen-negative escape. Recent studies have reported rapid progress in the engineering of dual-target CAR-T, incorporating diverse receptor architectures, logic-gated designs, and novel manufacturing platforms. Preclinical data demonstrate improved disease control across B-cell malignancies, acute myeloid leukemia, and autoimmune disease models. Here, we summarize the latest advancements in the preclinical investigations and clinical trials of dual-target CAR-T cell therapy presented at the 2025 ASH annual meeting.

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Development of super Vδ2 T cells for relapsed/refractory acute myeloid Leukemia via non-viral site-specific integration.

Liu Li L, Wang Hanlu H, Shi Lin L, Zhang Chao C et al.

The efficacy of chimeric antigen receptor (CAR)-T cell therapy in relapsed/refractory acute myeloid leukemia (R/R AML) is limited by tumor heterogeneity, antigen evasion, and treatment-related toxicities. Gamma delta (γδ) T cells mediate antitumor activity independent of MHC by sensing stress-induced ligands. A prominent mechanism involves NKG2D ligand (NKG2DL) recognition, which is highly upregulated in malignancies but generally low or restricted expression in healthy tissues under homeostatic conditions. In human peripheral blood, the Vδ2 subset represents the predominant population. Vδ2 T cells transduced with the NKG2D-CD3ζ construct, which incorporates into the natural γδ TCR/CD3 complex, preserve innate phosphoantigen recognition while acquiring potent NKG2DL-directed cytotoxicity, enabling dual-pathway tumor recognition. These cells are termed "Super Vδ2 T cells." We successfully generated TRAC-specific integrated Super Vδ2 T cells using CRISPR/Cas9 technology, achieving 90-93% CAR+ expression. In vitro assays demonstrated that the engineered "Super Vδ2 T cells" exhibited potent cytotoxic activity against multiple AML targets, including cell lines and primary R/R AML blasts, in contrast to their negligible toxicity on monocytes. In vivo, Super Vδ2 T cells demonstrated substantial tumor reduction without graft-versus-host disease (GvHD) reaction. Collectively, our data demonstrated that Super Vδ2 T cells represent a viable allogeneic therapy for AML.

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Tanshinone IIA impairs platelet function and thrombus formation.

Gu Wei W, Hu Haibo H, Zhu Wei W, Li Yuanyuan Y et al.

Tanshinone IIA (T-IIA) is a fat-soluble active ingredient derived from the traditional Chinese medicine Danshen and possesses cardioprotective property. However, its exact role in platelet function is unknown. This study investigated T-IIA's role in platelet aggregation, granules release, spreading, clot retraction as well as in vivo hemostasis and thrombus formation. Human platelets were treated with different doses of T-IIA (10, 50, and 100 μM) to measure platelet function and activation. In addition, T-IIA was administrated into wild-type mice to evaluate hemostasis and thrombus formation. T-IIA significantly impaired platelet aggregation, ATP secretion, P-selectin expression, spreading and clot retraction dose-dependently without affecting the expression profiles of αIIbβ3, GPVI, or GPIbα. Administration of T-IIA significantly prolonged mice tail bleeding time and inhibited arterial and venous thrombosis. Further analysis showed that T-IIA dose-dependently reduced platelet ROS generation. Quantitative proteomic and phosphoproteimic assays analyzing T-IIA-treated versus vehicle-treated platelets after stimulation identified dysregulated phosphorylation of several proteins, which were enriched in platelet activation. Among the downregulated phosphoproteins, Rho-associated protein kinase 1 (ROCK1), integrin β3 and talin1 exhibited the lower fold change of phosphorylation in T-IIA-treated platelets compared to vehicle. Consistently, T-IIA treatment inhibited the phosphorylation of ROCK1, p47phox, integrin β3 and talin1 in activated platelets. Tanshinone IIA impairs platelet function and thrombosis via inhibition of several signaling pathways including ROCK1/p47phox, β3 and talin1, implying that tanshinone IIA may represent a promising therapeutic candidate for treating thrombotic diseases.

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Chimeric antigen receptor T-cell (CAR-T) therapy was initially used to treat B-cell malignancies, and it is now considered an effective treatment option for multiple sclerosis (MS). CAR-T therapy selectively targets and depletes pathogenic B cells within lymphoid tissue and the central nervous system (CNS), showing promise for achieving deep, sustained remission and long-term treatment-free disease control in patients with refractory MS. A comprehensive analysis was carried out by searching multiple keywords with combinations such as "CAR-T", "MS", "Demyelination", "Autoimmunity", "CD19", "Inflammation", "B cells", T cells", "Neurodegeneration ", "Neurological Disorders", "Immunity", etc. The review included preclinical and clinical research articles publicly available till March 2026. This study was conducted to explore the mechanisms of action, clinical effectiveness, safety profile, and prospects for CAR-T treatment for MS. From the beginning clinical testing indicates that CD19 targeted CAR-T cells can efficiently and permanently destroy through B-cells, leading to a significant decrease in disease progression, a recovery of impairment, and an immense reduction in inflammatory markers in individuals who have progressive MS. New techniques for engineering such as allogeneic CAR-T cells and enhanced CRISPR-based safety switches, are being investigated for making things safer and easier for individuals. CAR-T treatment represents a revolutionary approach for individuals with refractory MS. With ongoing improvements in safety and specificity, it has the potential to transform the therapeutic paradigm toward a sustainable immunological reset and prolonged remission in clinical neuroimmunology.

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Neutralizing LFA-1 alleviates acute lung injury by diminishing pulmonary retention of CAR-T cells.

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On-target, off-tumor toxicity presents a significant challenge in chimeric antigen receptor (CAR) T therapy for solid tumors. Traditional approaches to managing adverse reactions, such as suppressing in vivo CAR-T cell activity, risk impairing their antitumor efficacy, often resulting in treatment failure. Intravenously infused CAR-T cells initially traffic to the lungs, where they are activated by tumor-associated antigens (TAAs) expressed on pulmonary tissues, leading to acute lung injury. To address this, this study developed a strategy involving leukocyte function-associated antigen 1 (LFA-1) neutralization at the time of infusion. This approach modulates CAR-T cell pharmacokinetics to enhance efficacy while minimizing toxicity. Post-infusion, CAR-T cells preferentially sequester and activate in the lung, secreting tumor necrosis factor α (TNF-α), which upregulates intercellular adhesion molecule 1 (ICAM-1) expression on pulmonary endothelial cells. This triggers an "activation-adhesion" feedback loop via the LFA-1/ICAM-1 pathway, exacerbating lung injury. Neutralization of LFA-1 during infusion significantly reduces CAR-T cell adhesion to pulmonary endothelium, disrupts this feedback loop, and mitigates acute lung injury. By accelerating the pharmacokinetic progression of CAR-T cells beyond the lung, this strategy not only alleviates the acute toxicity associated with high-dose regimens but also enhances the antitumor efficacy of low-dose CAR-T cells, thus expanding the therapeutic window.

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