Drug Database
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

PubMedJournal of the colleges of medicine of South Africa2026-11-11

The genetic profile of B-cell acute lymphoblastic leukaemia diagnosed in Pretoria, South Africa: A 10-year retrospective study.

Olivier Kirsten K, Marais Annelli A, Thompson Keryn K, Badenhorst Amery A et al.

B-cell acute lymphoblastic leukaemia (B-ALL) comprises genetically distinct subtypes with important prognostic implications. South African data suggest a different genetic landscape to other geographic regions, with a higher frequency of t(1;19). This study aimed to describe the genetic profile of B-ALL diagnosed at a South African tertiary haematology laboratory over a 10-year period. In this retrospective, descriptive study, all B-ALL cases (2014-2023) recorded in flow cytometry and cancer registries were identified. Demographic and laboratory data, including immunophenotypic and genetic findings, were extracted from the laboratory information system. Genetic work-up included karyotyping, a routine fluorescence in situ hybridisation panel: KMT2A rearrangement, t(1;19), t(12;21) and t(9;22), and real-time quantitative polymerase chain reaction where available. A total of 173 patients were included (54.9% male; 75.7% < 19 years). Genetic testing was requested in 146 cases (84.4%), with definitive results in 115 (78.8%). Among informative cases, t(1;19) was most frequent (26.1%), followed by t(9;22) (12.2%), t(12;21) (10.4%), high hyperdiploidy (9.6%), KMT2A rearrangement (7.0%) and hypodiploidy (0.9%). The t(1;19) translocation predominated in paediatric patients, while t(9;22) was more common in adults. Both t(12;21) and KMT2A rearrangements were restricted to patients < 19 years. This cohort demonstrates a high frequency of t(1;19) and age-specific variation in B-ALL genetic subtypes, suggesting a distinct regional genetic profile. Expanded diagnostic testing and multicentre African studies are needed to refine risk stratification and guide context-appropriate care. This study provides data on the distribution of selected genetic subtypes of B-ALL in a South African population, identifying differences in subtype frequency and age distribution that may inform regional diagnostic strategies and risk-directed care.

PMID 43011188
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PubMedFrontiers in immunology2026-11-11

Epigenomic insights into CD4+ T-cell-mediated pathogenesis in autoimmune diseases.

Goto Manaka M, Teruya Hiroyuki H, Okamura Tomohisa T, Fujio Keishi K

T cells are central mediators of autoimmune disease pathogenesis. After developing in the thymus, T cells undergo diverse differentiation programs and acquire specialized effector functions in inflamed tissues. Despite sharing the same genome, T cells adopt diverse phenotypes and functions, highlighting the importance of epigenetic mechanisms in regulating their differentiation and activity; however, these mechanisms remain incompletely understood. Comprehensive epigenetic analyses are therefore essential to elucidate these processes. To date, a wide range of approaches has been applied to T-cell research, including analyses of DNA methylation, histone modifications, chromatin accessibility, transcription factor binding, and three-dimensional chromatin architecture. More recently, rapid advances in single-cell technologies have enabled simultaneous profiling of gene expression and chromatin accessibility in the same cell. In parallel, CRISPR-based approaches have enabled genome-wide functional interrogation in primary human T cells, including analyses of non-coding regulatory regions. Furthermore, epigenomic approaches are now being applied to spatial analyses and are expected to provide deeper insight into the organization of T-cell states in inflamed tissues. In this mini review, we highlight recent studies that have leveraged these cutting-edge technologies and discuss how they are advancing our understanding of the T-cell-mediated pathogenesis of autoimmune diseases.

PMID 43011665
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PubMedFrontiers in immunology2026-11-11

Molecular mechanisms regulating T-cell receptor signaling and T-cell function.

Kurilin Vasily V VV, Fisher Marina S MS, Sennikov Sergey V SV

The T-cell receptor (TCR) is the central mediator of antigen-specific recognition and a key regulator of T-lymphocyte function. Current evidence indicates that TCR signaling is not a linear cascade but a multilevel dynamic system in which cellular responses are shaped by the combined effects of TCR-CD3 structural organization, spatial receptor distribution, the lipid microenvironment, mechanical forces, kinase and phosphatase activity, co-stimulatory and inhibitory receptors, cellular metabolic state, and the strength and duration of TCR interactions with peptide-MHC (pMHC) complexes. This review summarizes current concepts of the molecular and spatial organization of TCR-CD3; mechanisms of signal initiation involving Lck, CD45, SHP phosphatases, ITAMs, ZAP-70, and the LAT-SLP-76 signalosome; and the coupling of TCR signaling to T-cell metabolic programs. Particular attention is paid to the nonlinear relationship between functional responses, TCR affinity, and target pMHC density; the role of chronic antigenic stimulation in T-cell exhaustion and activation-induced cell death (AICD); and the involvement of NFAT-, TOX-, NR4A-, and TCF1-dependent programs in this process. We also discuss the translational relevance of these mechanisms to antitumor immunotherapy and the restoration of immune tolerance, including immune checkpoint blockade, CAR-T, TCR-T, and TCR-Treg approaches and CD3/TCR-directed T-cell-engager platforms. Finally, we consider the concept of TCR signal tuning, according to which therapeutic efficacy is determined not by maximal receptor signal strength but by an optimal balance between antigen sensitivity, specificity, effector activity, metabolic fitness, and the ability of T cells to retain function under sustained antigenic pressure.

PMID 43011816
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PubMedImmunology2026-11-11

Determinants of T Cell Exhaustion: How Far Back Can We Go?

Olumade Testimony T, Santer Deanna M DM, Arsenio Janilyn J

Over the past four decades, T cell exhaustion has been primarily associated with chronic infection and cancer and described as a late, adaptive response that limits immunopathology under chronic antigen exposure. Emerging evidence has revealed that exhausted T (Tex) cells are formed developmentally with distinct transcriptomic, epigenetic and phenotypic profiles, with progressive and hierarchical loss of effector functions. Recent reports show that exhaustion is not merely a late-stage phenomenon, but a multifaceted developmental trajectory that begins far earlier than previously thought. Intrinsic factors established at T cell priming synergize with extrinsic cues from the tissue microenvironment to drive T cell differentiation towards an exhausted state long before exhaustion becomes phenotypically fixed. This review presents an overview of recent knowledge that has reshaped our understanding of T cell exhaustion formation. Here, we discuss the genetic, epigenetic and metabolic determinants of T cell exhaustion, as well as the roles other soluble mediators and cell types may play in promoting exhaustion. Enhancing our understanding of early determinants of exhaustion has implications for the development and application of therapeutic strategies that adapt to the temporal evolution of exhaustion, which may be more effective than treatments aimed solely at reversing exhaustion.

PMID 43012642
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PubMedGenes and immunity2026-11-11

Understanding the phosphoantigen, butyrophilin, and γ9δ2 T cell axis.

Jin Yiming Y, Bashir Sidra S, Pawge Girija G, Hsiao Chia-Hung Christine CC et al.

The γ9δ2 T cells act at the intersection of innate and adaptive immunity to rapidly respond to infections and cancer. Over the past few decades, pivotal discoveries have clarified the mechanisms by which microbial and endogenous phosphoantigens (pAgs) bind to butyrophilins (BTNs), inducing conformational and clustering changes that facilitate γ9δ2 T cell activation. These discoveries involve advances in understanding pAg structure-activity relationships and identification of new natural and synthetic pAgs with diverse binding modes. Molecular and structural biology studies have led to the elucidation of the architecture of BTN complexes, such as the 3A1-3A2-(2A1)2 complex for (E)-4-hydroxy-3-methyl-but-2-enyl diphosphate (HMBPP) detection and the (3A3)2-(2A1)2 complex for mevalonate diphosphate (MPP) detection, and their engagement with γ9δ2 T cell receptors. Clinically, γ9δ2 T cells are being explored using synthetic pAgs, bisphosphonates, and BTN antibodies to expand and activate these cells. In this review, we examine the major milestones in research on the pAg, BTN, and γ9δ2 T cell axis, highlighting its significance to human cancers.

PMID 43009532
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PubMedFrontiers in oncology2026-11-11

Locally manufactured point-of-care CD19 chimeric antigen receptor T-cell therapy for paediatric relapsed/refractory B-cell acute lymphoblastic leukaemia: a single-centre feasibility experience.

Chan Wilson Yau Ki WYK, Leung Alex Wing Kwan AWK, Zhang Hui H, Cheuk Daniel Ka Leung DKL et al.

The high cost of commercial CD19-targeted chimeric antigen receptor T-cell (CAR-T) therapy for relapsed/refractory B-cell acute lymphoblastic leukaemia (B-ALL) is prohibitive for many centres and families worldwide. It is imperative to develop a cost-effective, high-quality local manufacturing system to make CAR-T a financially feasible point-of-care (POC) production option for patients. This was a single-centre, open-label, non-randomised phase II clinical trial aimed at evaluating the efficacy and safety of the locally manufactured autologous anti-CD19 CAR-T cells, generated using the CliniMACS Prodigy system, in the treatment of relapsed/refractory B-ALL. The production efficiency, efficacy, and toxicity of CAR-T therapy were evaluated. A total of 6 patients were recruited, including 3 male and 3 female patients. Five patients were recruited upon first relapse, while one was recruited upon second relapse. Two patients had central nervous system involvement upon relapse, as determined by flow cytometry (CNS2). The median age at CAR-T infusion was 9 years (range 4-14 years). The median time from the most recent relapse to CAR-T infusion was 5.33 months (range 4.58-5.83 months). The median percentage of blasts was 5% (range 3%-93%) in bone marrow before CAR-T infusion. All patients received intravenous cyclophosphamide 1,000 mg/m2 and fludarabine 120 mg/m2 for lymphodepletion. The median cell dose was 2.67 × 106 CAR-positive viable T cells/kg (range 2.3-2.95 × 106/kg). The median transduction efficiency was 42.86% (range 33.89%-62.1%) and the median viability of CD3+ cells was 96.22% (range 95.61%-96.78%). The median viral copy number was 2.03 (range 1.72-2.48). All products were intact with no visible damage or leakage. The median filled volume per bag was 28.96 mL (range 15.8-64.01), with a median number of viable CAR-T cells of 76 × 106 cells (range 47 to 174 × 106 cells) and a median concentration of viable CAR-T cells of 2.71 × 106/mL (range 2.41-2.99 × 106/mL). No aggregates or endotoxins (<0.500 EU/mL) were detected in any of the products. Tests for bacterial growth and mycoplasma by quantitative PCR (qPCR) were all negative. Five patients experienced grade 1 cytokine release syndrome (CRS), while one patient experienced grade 3 CRS. CRS occurred at a median of 1.5 days (range 0-6 days) after infusion and resolved by a median of 6.5 days (range 5-16 days) after infusion with the use of a median of 3 doses (range 1-8 doses) of tocilizumab. At a median follow-up of 9 months, all patients remained in remission. The median progression-free survival was not reached. All patients were administered intravenous immunoglobulin replacement every 4 weeks after CAR-T infusion. Locally manufactured POC CAR-T may be a feasible option for providing potentially safe, timely, and cost-effective therapy for B-ALL upon first relapse, based on preliminary Hong Kong data from a small number of patients. Further validation in larger studies is recommended to validate scalability, long-term persistence, and cost-effectiveness.

PMID 43011663
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