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T-

T-Bactum (EB23 18235Y / EB2318235Y)

✓ Approved

Essex Bio-Technology Limited · therapeutic agent

What is T-Bactum?

T-Bactum is a therapeutic agent developed by Essex Bio-Technology Limited. It is approved for therapeutic indications via oral (po).

Drug Profile

Brand NamesEB23 18235Y, EB2318235Y
CompanyEssex Bio-Technology Limited
RouteOral (PO)
StatusApproved
Sources: ClinicalTrials.gov, Essex Bio-Technology Limited

Therapeutic Indications

T-Bactum is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Infections and infestationsOral infection✓ Approved

Related Research Articles

PubMedJCI insight2026-06-09

Reduced CCL/Be-specific CD4+ T cells in CCL3-deficient or peptide-MHC II CAR-T cell-treated mice.

Falta Michael T MT, Raza Masoom M, Nevienski Caley J CJ, Brunetti Tonya M TM et al.

In chronic beryllium disease (CBD), elevated levels of the inflammatory chemokines CCL3 and CCL4 in the lungs coincide with expanded populations of CD4+ T cells specific to beryllium (Be)-modified peptides derived from these chemokines. Here, we generated HLA-DP2 transgenic (Tg) CCL3-deficient mice (CCL3-/-) that also lack CCL4 to investigate their role in disease development. Be-exposed CCL3-/- mice maintained normal numbers of lung macrophages and dendritic cells (DCs) but exhibited significantly reduced total and HLA-DP2-CCL/Be tetramer-specific CD4+ T cells, IFN-γ-producing CD4+ T cells, and peribronchovascular aggregates, consistent with attenuated inflammation. CCL3 was predominantly expressed in macrophages and DCs, and bone marrow chimera studies confirmed that hematopoietic-derived DCs are the key regulators of CCL/Be-specific CD4+ T cell responses. RNA sequencing of lung-resident CCL4/Be tetramer-positive CD4+ T cells revealed a transcriptional profile enriched for inflammatory and cholesterol-metabolism pathways, with elevated expression of Ifng, Tnf, and Il17a. Moreover, Be-exposed HLA-DP2 Tg mice lacking TNF-α or treated with peptide-MHCII CAR-T cells targeting CCL4/Be-specific CD4+ T cells showed reduced T cell responses and cellular aggregates. These findings demonstrate that CCL3 and CCL4 promote CCL/Be-specific CD4+ T cell responses and highlight peptide-MHCII CAR-T cells as a novel strategy for depleting self-peptide/Be-specific CD4+ T cells in CBD.

PMID 42262522
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PubMedEMBO molecular medicine2026-06-09

Functional screening of TCR-like antibodies using STAR-T cell library for cancer immunotherapy.

Li Yi Y, Huang Daosheng D, Liu Chang C, Zhou Zhixiao Z et al.

Adoptive T-cell therapies engineered with T-cell receptors (TCRs) or TCR-like antibodies have shown considerable promise in cancer immunotherapy. However, identifying tumor antigen-specific TCR-like antibodies, particularly against human leukocyte antigen-presented neoantigens, remains challenging. Here, we present a function-based, rather than affinity-based, antibody screening platform utilizing Synthetic T-cell receptor and Antigen Receptor (STAR)-T cell libraries. We found that antigen engagement in STAR-T cells triggers synchronous receptor endocytosis and T-cell activation, and we integrated these paired processes into an Endocytosis-Activation (E-A) functional readout for antibody screening. Applying E-A functional screening, we rapidly identified multiple nanobodies targeting the cell-surface antigen CD22 as well as the intracellular neoantigen P53R175H. STAR-T cells engineered with these nanobodies mediated potent anti-tumor efficacy both in vitro and in vivo. Furthermore, this platform yielded nanobodies that can be directly reformatted into other therapeutic modalities, including chimeric antigen receptors and bispecific antibodies, while maintaining cytotoxic function. Overall, the E-A screening platform links antibody discovery directly to T-cell function, providing a robust approach for identifying therapeutic antibodies, especially neoantigen-specific nanobodies, for T cell-based cancer immunotherapy.

PMID 42260138
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PubMedJournal of immunology research2026-06-09

Metabolic Reprogramming of T Cells by MSCs Rebalances Th17/Treg Axis to Attenuate Collagen-Induced Arthritis.

Wang Xiaoping X, He Jingjing J, Wang Qun Q, Liu Xue X et al.

Rheumatoid arthritis (RA) is a chronic autoimmune disorder characterized by dysregulated T cell responses and metabolic disturbances. Mesenchymal stromal cells (MSCs) have shown therapeutic promise, but their mechanisms, particularly concerning T cell metabolism, remain incompletely defined. This study investigated whether human umbilical cord-derived MSCs (hUC-MSCs) ameliorate collagen-induced arthritis (CIA) by modulating T cell metabolism and differentiation. CIA was induced in DBA/1 mice. Animals received PBS or hUC-MSCs on day 28. Arthritis index (AI), joint histology, serum cytokines (TNF-α, IL-6, IL-17, and TGF-β), and metabolites (lactate and pyruvate) were assessed. Splenic T cell transcription factors (FOXP3, RORγt, and PU.1) and glycolytic genes (GLUT1, G6PD, and PFKFB3) were analyzed by real-time quantitative polymerase chain reaction (RT-qPCR) and western blot. In vitro, human CD4+ T cells were cocultured with hUC-MSCs under T-helper 17 (Th17)-polarizing conditions. T cell subsets, glycolytic metabolites, and gene/protein expression were evaluated by flow cytometry, colorimetric assays, RT-qPCR, and western blot. MSC treatment significantly attenuated arthritis severity, joint destruction, and splenomegaly in CIA mice. It reduced serum pro-inflammatory cytokines and normalized elevated lactate and pyruvate levels. In the spleen, MSCs suppressed RORγt and PU.1 while enhancing FOXP3 expression, and downregulated GLUT1 and G6PD mRNA. Positive correlations were found between glycolytic markers (GLUT1 and G6PD) and pro-inflammatory transcription factors (RORγt and PU.1), and between serum lactate and inflammatory cytokines. In vitro, hUC-MSCs directly inhibited Th17 differentiation and promoted Treg generation in human CD4+ T cells. This metabolic reprogramming was functionally coupled to a shift in T cell differentiation: a suppression of pro-inflammatory Th17 cells and a promotion of regulatory T (Treg) generation in human CD4+ T cells. This was accompanied by reduced lactate production and significant downregulation of GLUT1, G6PD, and PFKFB3 at both mRNA and protein levels. hUC-MSCs ameliorate CIA by restoring the Th17/Treg balance through metabolic reprogramming of T cells, specifically by suppressing glycolysis. This immunometabolic mechanism highlights the therapeutic potential of MSCs in RA.

PMID 42260739
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PubMedMolecular immunology2026-06-09

Combined targeting of mesothelin and tenascin-C enhances CAR-T cell function and tumor microenvironment modulation in ovarian cancer.

Wang Xiaoqin X, Zhang Duoyi D, Wang Tingting T, Li Xin X et al.

The efficacy of chimeric antigen receptor T (CAR-T) cell therapy in solid tumors is limited by dense extracellular matrix deposition and an immunosuppressive tumor microenvironment. Tenascin-C (TNC), an extracellular matrix protein enriched in ovarian cancer stroma, may provide a stromal cue that restricts T-cell engagement while offering a complementary target to mesothelin (MSLN). This study evaluated whether combined targeting of MSLN and TNC could enhance CAR-T-cell function and remodel the ovarian cancer microenvironment. CAR-T cells targeting MSLN and/or TNC were generated using single lentiviral vectors encoding second-generation CAR constructs, including tandem dual-target CARs and MSLN-directed CAR-T cells secreting an anti-TNC single-chain variable fragment with or without a membrane-tethered PD-L1-binding module. CAR expression and function were evaluated across three healthy-donor batches. Target expression on SKOV3 cells and ovarian cancer-associated fibroblasts (CAFs) was validated by flow cytometry and qPCR. Functional studies included NFAT reporter assays, cytokine release, cytotoxicity, immune synapse quantification, adhesion assays, CAF co-culture, and xenograft studies with randomized treatment allocation and blinded tumor measurements. Dual-target TNC+MSLN CAR-T cells demonstrated reproducible CAR expression across donors, enhanced NFAT activation in TNC-rich conditions, increased CD69/CD25 upregulation, and greater IFN-γ, TNF-α, and IL-2 secretion than single-target controls. Compared with MSLN-CAR-T cells, dual-target CAR-T cells showed improved tumor-cell killing, larger and more polarized immune synapses, and stronger tumor-cell adhesion. In CAF co-culture, anti-TNC-secreting CAR-T cells partially reversed suppression, reduced PD-1 and Tim-3 expression, and showed concordant reductions in LAG-3 and TIGIT in exploratory analyses. In vivo, combination stromal targeting delayed tumor growth, increased intratumoral CD4 + and CD8 + infiltration, improved CAR-T persistence, and reduced extracellular matrix deposition and CAF-associated markers. Combined targeting of MSLN and TNC was associated with improved CAR-T-cell activation and broader microenvironmental remodeling in ovarian cancer models. These data support further evaluation of stromal co-targeting as an adjunct strategy for CAR-T therapy in ovarian cancer, while additional validation of target dependence, safety, and long-term persistence remains necessary.

PMID 42259008
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PubMedJournal of immunotherapy (Hagerstown, Md. : 1997)2026-06-09

Ligand-Receptor-Based Novel TWEAK CAR-T Exhibits Potent Antitumor Activity Against Liver Cancer by Targeting FN14.

Bai Zhiyong Z, Deng Jian J, Fang Lisha L, Liu Nan N et al.

Liver cancer is the most frequent fatal malignancy, and existing treatments have limited efficacy. Tumor necrosis factor receptor superfamily member 12A (FN14) is highly expressed in liver cancer cells and promotes tumor cell proliferation, migration, invasion, and angiogenesis, suggesting that FN14 is a suitable therapeutic target for liver cancer. As a targeted therapy, chimeric antigen receptor T (CAR-T) cells have demonstrated potential for treating solid cancers. We designed a CAR targeting FN14 based on the extracellular domain of tumor necrosis factor superfamily member 12 (TWEAK), the only natural ligand for FN14, and tested its cytotoxic effect on tumor cells in vitro and in vivo. The results show that multiple liver cancer cell lines exhibit high FN14 expression. TWEAK-CAR-T cells specifically and effectively kill these cells in vitro. TWEAK-CAR-T cells also significantly suppress the growth of SK-Hep1 xenografts with high T-cell infiltration in the tumor. Moreover, potent and broad cytotoxicity of TWEAK-CAR-T was observed against diverse tumor cell lines from multiple cancer types. Our findings indicated that TWEAK-CAR-T cell therapy may be an effective therapeutic strategy for liver cancer.

PMID 42262411
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PubMedEuropean journal of immunology2026-06-09

Identifying Negative Biomarkers of CD4 Cytotoxic T Lymphocytes via Granzyme B Exclusion Analysis.

Wang Bingsu B, Bahabayi Ayibaota A, Huang Danyi D, Xiong Ziqi Z et al.

CD4 cytotoxic T lymphocytes (CTLs) are a distinct subset of CD4+ T cells that can mediate antigen-specific cytotoxicity. However, their specific surface markers have yet to be defined. In this study, we used gene-plasticity-based mutual exclusion analysis to identify negative biomarkers for CD4 CTLs, using granzyme B (GZMB) expression as the pivotal reference. We analyzed bulk RNA-seq data from 768 human CD4+ T cell samples, calculated gene plasticity scores, and applied cosine similarity to detect genes that are anti-correlated with GZMB. Several genes encoding cell surface membrane proteins were identified as important candidates. ITGA6 (CD49f) and IL6R (CD126) were validated by flow cytometry in healthy individuals and primary Sjögren's syndrome (pSS) patients. The expression profile confirmed mutually exclusive between GZMB and both CD49f and CD126, with CD49f-CD126-GPR56+ CD4+ T cells exhibiting the highest GZMB levels. In pSS patients, CD49f-CD126-GPR56+ cells in CD8+ T cells were significantly negatively correlated with clinical parameters (IgA, anti-SSB). ROC analysis revealed the percentages of GZMB in CD4+ T cells (AUC = 0.766) and GPR56/GZMB in CD8+ T cells (AUC = 0.76) as diagnostic biomarkers.

PMID 42261594
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