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

PubMedAnnales de pathologie2026-07-17

[Diagnostic approach to non-cutaneous T-cell lymphomas in 2025: What pitfalls and how should they be classified?]

Drieux Fanny F, Pirlog Radu R, Gaulard Philippe P, Poullot Elsa E

Peripheral T-cell lymphomas are a heterogeneous group of neoplasms derived from mature T or NK lymphocytes. With the exception of primary cutaneous T-cell lymphomas, these lymphomas are rare (<7% of lymphomas in France). Peripheral T-cell lymphomas derived from follicular helper T cells (TFH) account for more than 40% of cases. TFH lymphoma has numerous diagnostic pitfalls, including classical Hodgkin lymphoma, diffuse large B-cell lymphoma, and marginal zone lymphoma, which are attributable to the "follicular T helper" function of the tumor cells. Anaplastic large cell lymphomas (ALCL) are classified according to the presence or absence of an ALK gene fusion (ALCL-ALK+) and, for ALCL ALK-, according to their clinical presentation as nodal, cutaneous, or breast implant-associated disease. Among intestinal peripheral T-cell lymphomas, classifications distinguish enteropathy-associated T-cell lymphoma and monomorphic epitheliotropic intestinal T-cell lymphoma, two diseases derived from intraepithelial intestinal T lymphocytes that differ in their clinical context, immunomorphological features, and distinct mutational profiles. Assessment of Epstein-Barr virus (EBV) status is a fundamental prerequisite in peripheral T-cell lymphomas. Among extranodal peripheral T-cell lymphomas, EBV association defines extranodal NK/T-cell lymphoma. This review will address the diagnostic approach to a T-cell infiltrate, the various T cell lymphoma entities according to nodal, extranodal, or leukemic presentation, the main differential diagnoses, and the diagnosis of exclusion, peripheral T-cell lymphoma, not otherwise specified. With a few exceptions, peripheral T-cell lymphomas are aggressive diseases for which conventional chemotherapies are of limited efficacy.

PMID 42463321
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PubMedbioRxiv : the preprint server for biology2026-07-17

CXCR6 marks polyfunctional effector CD4 T cells required for anti- Chlamydia immunity in the female reproductive tract.

Mercado Miguel A B MAB, Kim Yejin Y, Li Qiang Q, Li Lin-Xi LX

CD4 T cells are essential for protective immunity against Chlamydia in the female reproductive tract (FRT), yet the characteristics of protective mucosal effector CD4 T cells remain poorly defined. We previously identified the transcription factor BHLHE40 as a key regulator of polyfunctional effector CD4 T cell differentiation during Chlamydia infection. Here, we identify the chemokine receptor CXCR6 as a marker of these protective T cells. Following intravaginal Chlamydia muridarum infection, Bhlhe40 -deficient mice exhibited reduced frequencies of CXCR6⁺ CD4 T cells that correlated with impaired bacterial control. CXCR6 expression on T cells was associated with loss of stem-like features and acquisition of an effector phenotype. Compared with CXCR6⁻ cells, CXCR6⁺ CD4 T cells displayed enhanced proliferation and polyfunctionality by co-producing cytokines IFN-γ, IL-17A, and GM-CSF. Although CXCR6 was dispensable for CD4 T cell homing to the FRT, it promoted localization to the infected epithelium and the emerging memory lymphoid clusters. Importantly, depletion of CXCR6⁺ CD4 T cells reduced polyfunctional effectors and impaired bacterial clearance. Collectively, these findings identify CXCR6 as a marker of protective polyfunctional CD4 T cells and implicate CXCR6-dependent tissue positioning as a key component of effective mucosal immunity, highlighting CXCR6 as a potential biomarker for Chlamydia vaccine development.

PMID 42465284
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PubMedbioRxiv : the preprint server for biology2026-07-17

NK-like and networked CD8 + T cell immunity mediates exceptional HIV control.

Alrubayyi Aljawharah A, Traunbauer Anna K AK, Crain Charles R CR, Bhattacharyya Shaown S et al.

Durable treatment-free remission remains a defining goal for people living with HIV (PLWH). Studies of spontaneous elite controllers have revealed that functional CD8⁺ T cells targeting structurally networked viral epitopes can mediate durable viral suppression 1,2 . However, rare reservoir-defined exceptional controllers within the spectrum of elite control 3-5 , characterized by the absence of intact provirus or proviruses confined to transcriptionally repressed genomic regions 6 , provide a unique opportunity to define mechanisms of cure-like immunity. Here, we integrate functional epitope mapping, single-cell transcriptomics, and infected cell elimination assays to identify networked HIV epitope targeting and a natural killer (NK)-like killer-cell immunoglobulin-like receptor (KIR)⁺ CD8⁺ T cell subset as key features of exceptional control. This NK-like subset was selectively enriched within HIV-specific, but not CMV-specific, CD8⁺ T cells from controllers, and was transcriptionally similar to highly cytotoxic subsets within the broader KIR + CD8 + T cell compartment. Flow cytometry revealed increased frequencies of KIR⁺ CD8⁺ T cells in exceptional controllers relative to antiretroviral therapy (ART)-suppressed individuals, and unexpectedly, enrichment of dual KIR + NKG2A + CD8⁺ T cells. Functional depletion of KIR⁺ CD8⁺ T cells significantly impaired the elimination of autologous HIV-infected CD4⁺ T cells, despite preserved recognition by proliferative networked HIV-specific CD8⁺ T cells. These findings thereby identify an NK-like KIR⁺ CD8⁺ T cell state as a previously unrecognized component of exceptional HIV immunity that complements networked epitope targeting, providing a novel framework for immunotherapeutic HIV cure strategies.

PMID 42465352
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PubMedbioRxiv : the preprint server for biology2026-07-17

Bcl11b dose-dependently regulates positive selection of CD8 T cells to the virtual memory fate.

Sidwell Tom T, Rothenberg Ellen V EV

Virtual memory T cells are increasingly recognized as a functionally distinct lineage within the CD8 T cell pool, but when and how commitment to the lineage is enforced remain poorly understood. Here we demonstrate that T VM lineage choice is exceptionally sensitive to dosage and repression competence of the key T cell transcription factor Bcl11b. Three different genetic models of slightly reduced Bcl11b each biased CD8 cell development to T VM generation without deregulating effector differentiation. Timed conditional knockouts and adoptive transfers narrowed the developmental window and showed that Bcl11b levels determine diversion to virtual memory fate uniquely during intrathymic positive selection. Whereas total Bcl11b loss disrupts TCR signalling, a <2-fold dose reduction of Bcl11b enhanced selective responses to TCR stimulation. Chromatin accessibility profiling and single cell RNA-seq indicated that Bcl11b dose reduction redirects cells to the T VM fate, from the late cycling fraction of mature CD8SP thymocytes, by a mechanism independent of previously described cytokine-driven pathways.

PMID 42465258
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PubMedbioRxiv : the preprint server for biology2026-07-17

Confined T cell migration controls programmed cell death 1 expression.

Alapan Yunus Y, Kim Jaehoon J, Min Kiyoon K, Shih Alexander A et al.

T cell immune checkpoint expression and dysfunction are attributed solely to molecular cues. We discover using microphysiological systems and in vivo models that transmigration through confined pores induces acute loss of programmed cell death 1 within minutes of surface immune checkpoint markers on CD8+ T cells through ubiquitin-mediated proteasomal degradation, corresponding with enhanced fitness and function. Such imprints and its underlying mechanism of programmed cell death 1 loss are conserved across species and applicable to human TIL and CAR T cells, and are correlative with disease outcomes in human melanoma. Our findings establish the diverse tissues landscapes that T cells traverse during immunosurveillance, and specifically transmigration, as a form of mechanical immune regulation, and reveal a mechano-modulatory strategy to improve the quality and persistence of engineered or patient-derived T cells for adoptive immunotherapy.

PMID 42465295
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PubMedbioRxiv : the preprint server for biology2026-07-17

Restricted MHC-II trafficking in Mycobacterium tuberculosis -infected M2-like macrophages limits CD4+ T cell activation.

Sandhu Avinaash K AK, Gail Daniel P DP, Simmermon Rachel C RC, Webb Demetria D et al.

Recognition of infected macrophages by CD4+ T cells is essential to immune protection against Mycobacterium tuberculosis (Mtb), the causative agent of tuberculosis (TB). However, not all infected macrophage subsets successfully elicit T cell activation. We recently discovered that M2-like macrophages fail to efficiently activate memory CD4+ T cells when infected with Mtb, yet successfully elicit T cell activation when loaded with peptides, γ-irradiated bacteria, or Mtb whole cell lysate. Since the mechanisms underlying CD4+ T cell evasion by infected M2 but not M1-like macrophages remain underexplored, we sought to determine the genes and pathways unique to Mtb infection of M2-like cells, including alveolar macrophages. RNA sequencing of human macrophages infected with virulent Mtb identified enrichment of IL-10 and type I interferon (IFN) signaling genes, including IL10RA and HERC5 , respectively, in infected M2-like monocyte-derived and alveolar macrophages. However, genes involved in MHC-II trafficking, such as AP1M2 , were higher in infected M1-like macrophages. In complementary experiments using fluorescence microscopy and flow cytometry, we observed impaired trafficking of newly synthesized MHC-II to the plasma membrane of Mtb-infected M2-like macrophages despite high total surface MHC-II levels. Neutralization of IL-10 or knockdown of HERC5 restored MHC-II trafficking to the cell surface among infected M2-like macrophages and significantly enhanced activation of memory CD4+ T cells in an MHC-II-dependent manner. These findings identify coordinated IL-10 and type I IFN signaling as key mechanisms that restrict MHC-II trafficking to the plasma membrane in Mtb-infected M2-like macrophages, thereby limiting antigen presentation and CD4+ T cell activation. We propose that host-directed therapies targeting these pathways in infected alveolar macrophages will facilitate T cell recognition for the prevention or treatment of active TB. Recognition of infected macrophages by CD4+ T cells is essential to immune protection against Mycobacterium tuberculosis (Mtb), the causative agent of tuberculosis (TB). However, not all infected macrophage subsets successfully elicit T cell activation. We recently discovered that M2-like macrophages fail to efficiently activate memory CD4 + T cells when infected with Mtb, yet they successfully elicit T cell activation when treated with peptides, γ-irradiated bacteria, or Mtb whole cell lysate. In this study, we identified genes and pathways uniquely upregulated in Mtb-infected M2-like macrophages that are linked to inefficient CD4+ T cell activation, including IL-10 signaling and type I interferon (IFN) pathways. These pathways were linked to reduced MHC-II trafficking to the plasma membrane in Mtb-infected M2-like macrophages. Neutralization of IL-10 or knockdown of HERC5 restored MHC-II trafficking and augmented memory CD4+ T cell activation. Our study demonstrates that IL-10 signaling and type I IFN pathways play detrimental roles in macrophages during Mtb infection, impairing MHC-II trafficking and CD4+ T cell activation. Since lung-resident alveolar macrophages express a dominant M2-like phenotype, these findings suggest that targeting IL-10 and type I IFN signaling may offer a strategy to enhance CD4+ T cell-mediated immunity and improve TB outcomes.

PMID 42465483
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