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

PubMedBritish journal of cancer2026-09-20

TSPAN32 enhances CAR-T cell potency by assembling IL-2 receptor complex and amplifying its intracellular signal transduction.

Sun Yuanyuan Y, Qiu Qiang Q, Wang Bochuan B, Feng Yunyu Y et al.

Chimeric antigen receptor-engineered T cells (CAR-T) have shown substantial therapeutic potential in hematologic malignancies, but further improvement in T-cell functional capacity is needed to optimize efficacy. We observed reduced TSPAN32 expression in T cells from peripheral blood of patients with B-cell lymphoma. This study aimed to investigate whether TSPAN32 enhances CAR-T cell antitumor activity and to explore the underlying mechanism. TSPAN32 expression was assessed in T cells isolated from patients with B-cell lymphoma. T cells were engineered to co-express TSPAN32 and CD19-CAR, and their antitumor efficacy and cytokine secretion were evaluated in vitro and in subcutaneous tumor models in vivo. Gene expression profiling was performed to identify signaling pathways associated with TSPAN32 overexpression. Mechanistic studies examined the interaction between TSPAN32 and CD25 and its effect on IL-2 signaling. In addition, a transgenic mouse model with endogenous TSPAN32 overexpression and a TSPAN32-specific antibody (FF-37) were used to assess therapeutic potential. TSPAN32 expression was reduced in T cells from B-cell lymphoma patients. Co-expression of TSPAN32 with CD19-CAR significantly enhanced antitumor activity and cytokine production compared with CD19-CAR alone in vitro. In vivo, T cells engineered with both CAR and TSPAN32 showed superior therapeutic efficacy in subcutaneous tumor models. Gene expression profiling indicated increased IL-2 signaling activation in TSPAN32-high CAR-T cells. Mechanistically, TSPAN32 interacted with CD25, promoting its aggregation on the T-cell surface and enhancing IL-2 signal transduction. Endogenous TSPAN32 overexpression in transgenic mice increased resistance to subcutaneous tumor growth. Furthermore, the TSPAN32-specific antibody FF-37 increased TSPAN32 expression and improved CAR-T antitumor efficacy. TSPAN32 enhances CAR-T cell antitumor function by promoting CD25 aggregation and IL-2 signaling activation. Increasing TSPAN32 expression, either through genetic engineering or the TSPAN32-specific antibody FF-37, may represent a promising strategy to improve CAR-T cell therapy.

PMID 42763309
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PubMedJournal of inflammation research2026-09-20

Dimethyl Sulfoxide Modulates T Cell-Mediated Immunity to Attenuate Influenza A Virus Infection.

Jeng Po-Hsuan PH, Tsai Meng-Wei MW, Huang Shing-Hwa SH, Huang Tien-Ru TR et al.

Influenza A virus (IAV) remains a major threat because vaccines provide limited cross-protection and antiviral resistance is rising. Dimethyl sulfoxide (DMSO) is immunomodulatory, but its effect on IAV has not been tested in vivo. We evaluated its efficacy and mechanism in a murine H1N1 model. Male C57BL/6 mice were intranasally challenged with an LD50 of A/Puerto Rico/8/1934 (H1N1) and given daily subcutaneous DMSO (0.22 g/kg/day) or phosphate-buffered saline (PBS) on days 1-7. Survival was monitored for 21 days; lung and bronchoalveolar lavage fluid (BALF) were collected on day 8. Lung histology (hematoxylin and eosin), BALF cytokines (sandwich ELISA), lung and splenic IFN-γ-producing CD4+ and CD8+ T cells (flow cytometry), and whole-lung RNA sequencing (differential expression, KEGG enrichment) were assessed. BALF viral burden was measured by neuraminidase activity assay and TCID50. In vitro, splenic CD8+ T cells exposed to 0%, 0.5%, or 1.0% DMSO were immunoblotted for lymphocyte-activation gene 3 (LAG3). DMSO significantly improved 21-day survival and attenuated alveolar inflammatory infiltration. Day-8 BALF viral titers were significantly lower with DMSO (mean 2.2×103 vs 4.3×104 TCID50/mL; p = 0.034), as was neuraminidase activity. BALF IFN-γ and TGF-β were elevated, whereas TNF-α, IL-6, and IL-1β were not. IFN-γ+ CD8+ T cells increased in the lung but not the spleen; CD4+ populations were unchanged. RNA sequencing showed enrichment of cytokine-cytokine receptor interaction and PI3K/Akt signaling and upregulation of T-box factors, PPAR-γ, and Nek kinases. In vitro, DMSO accelerated LAG3 induction in CD8+ T cells within 12-48 h. DMSO is associated with attenuated IAV severity, a lower day-8 airway viral burden, and a localized expansion of IFN-γ-producing CD8+ T cells, without a concomitant rise in the pro-inflammatory cytokines TNF-α, IL-6, or IL-1β. These associations are correlative and support further investigation of DMSO as a host-directed adjunct for influenza.

PMID 42763701
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PubMedCase reports in genetics2026-09-20

Expanding the Progeroid Laminopathy Spectrum: Clinical Variability and Later-Onset Phenotype in Homozygous LMNA c.1579C>T (p.Arg527Cys) Associated Mandibuloacral Dysplasia.

Arany Eszter Sara ES, Zocche David D, Cobben Jan J

Homozygous LMNA c.1579C>T p.(Arg527Cys) has previously been reported in seven families and is associated with a progeroid phenotype intermediate between Hutchinson-Gilford progeria syndrome (HGPS) and mandibuloacral dysplasia type A (MAD-A). Due to the limited number of reported cases, the complete phenotypic spectrum associated with this variant remains poorly understood. Here, we describe two Syrian siblings born to consanguineous parents, both homozygous for the LMNA p.Arg527Cys variant. Unlike previously reported cases, these siblings demonstrated a notably delayed onset of clinical symptoms. Both patients exhibited severe generalized lipodystrophy, pronounced progeroid facial dysmorphism, mandibular hypoplasia with severe micrognathia, and pan-digital acro-osteolysis. Our findings expand the recognized clinical spectrum associated with the homozygous LMNA p.Arg527Cys variant and illustrate intrafamilial variability in age of onset within an otherwise relatively homogeneous phenotype.

PMID 42763606
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PubMedCurrent health sciences journal2026-09-20

The Assessment of T-Lymphocytes In Gastric Adenocarcinomas.

Pisică-Ilinca Roxana-Andreea RA, Stanca Liliana L, Zorilă Marian Valentin MV, Stepan Alex Emilian AE

Gastric adenocarcinomas (GAC) are common cancers in pathology, which pose real problems in practice due to heterogeneity, response to treatment and prognosis. New therapeutic approaches in GAC are aimed at activating the immune system by unblocking or modulating it. In this study, we analyzed the density and distribution of intra- and peritumoral CD4 and CD8 lymphocytes, by immunohistochemistry, in relation to the main prognostic parameters of GAC. CD4 and CD8 lymphocytes were superior in the tumor compartments in the case of discohesive and mixed GAC. They also predominated in discohesive GAC with signet ring cells at the intratumoral level and in those without other specifications at the peritumoral level. CD4 and CD8 were superior in high-grade GAC, in stages II/III and with lymphovascular invasion, more frequently peritumoral. The study indicated differences in the distribution of CD4 and CD8 T lymphocytes that may be useful for improving patient stratification for personalized targeted therapy of GAC.

PMID 42763754
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PubMedCureus2026-09-20

Candidate MicroRNA Regulatory Axes in Melanoma CD8+ T Cell Exhaustion: A Network-Based In Silico Stratification.

Javed Muhammad Zain U MZU, Hussain Muhammad M

Background Anti-programmed cell death protein-1 (anti-PD-1) immunotherapy has transformed the treatment of advanced melanoma, but durable benefit remains limited to a subset of patients. CD8+ T cell exhaustion contributes to immune escape in the melanoma tumor microenvironment, while the post-transcriptional regulation of exhaustion-associated genes by microRNAs (miRNAs) remains incompletely understood. Objective We characterized miRNA-mRNA regulatory associations in CD8+ T cell exhaustion-enriched melanoma transcriptomes, classified inverse associations as loss-of-repression (LoR) or active suppression (AS), extended the network to candidate long non-coding RNA (lncRNA)-miRNA-mRNA relationships, and examined whether network-derived transcriptomic scores were associated with anti-PD-1 outcomes in independent cohorts. Methods The TCGA-SKCM bulk transcriptomes were filtered by single-sample gene set enrichment analysis (ssGSEA), yielding 121 CD8+ T cell exhaustion-enriched cases and 115 cases with paired miRNA and mRNA measurements. Differentially expressed miRNAs (DEmiRNAs) were identified between fixed high- and low-exhaustion tertiles (n = 38 each) using two-sided Mann-Whitney U tests with Benjamini-Hochberg correction (|log₂FC| ≥ 0.5; false discovery rate (FDR) ≤ 0.05). Database-supported inverse Spearman's correlations (ρ ≤ -0.30; FDR ≤ 0.05) were assembled into a bipartite network. Edges were classified as LoR or AS, and a competing endogenous RNA (ceRNA) extension incorporated DIANA-LncBase/ENCORI lncRNA-miRNA interactions. Nine biologically anchored axes underwent continuous-score analysis and HC3 regression adjusted for tumor purity, CD8, fibroblast/CAF, myeloid, interferon-gamma, and sample type, together with four sensitivity analyses. Exploratory clinical testing used GSE78220 and the pre-PD-1 biopsy subset of the DFCI melanoma cohort (cBioPortal study identifier: mel_dfci_2019). Results Twenty-six DEmiRNAs (20 upregulated and 6 downregulated) formed 326 inverse miRNA-mRNA edges, comprising 263 AS and 63 LoR associations. Six of nine focused axes met the adjusted-support criterion, and all six were AS-classified including upregulated miR-155-5p as the dominant hub, with inverse associations involving FOXO3 (ρ = -0.305, adjusted p = 0.020) and MEIS1, the strongest priority edge (ρ = -0.470, adjusted p < 0.0001). NEAT1, MALAT1, and XIST emerged as the top-degree lncRNA hubs, all classified as AS-sponge type. Exclusion of one solid-tissue-normal specimen left 114 paired tumors, retained 25 DEmiRNAs, and supported seven of nine axes in the tumor-only sensitivity analysis. Relational integration with lncRNA-miRNA records yielded 29,274 candidate chains, including 790 containing a focused miRNA-mRNA edge. Transcriptomic score analyses were negative and exploratory in GSE78220 (mRNA proxy area under the curve (AUC) = 0.631; Mann-Whitney p = 0.269) and in the DFCI melanoma cohort (mRNA topology AUC = 0.453, p = 0.451; lncRNA topology AUC = 0.388, p = 0.0695). Conclusions The LoR/AS framework offers a transparent means of organizing correlative miRNA-mRNA hypotheses in melanoma bulk transcriptomes. The adjusted results favored an AS pattern among the focused axes, but they did not establish CD8+ T-cell-intrinsic regulation, direct miRNA targeting, ceRNA activity, or clinical predictive utility. Experimental testing in sorted or single-cell melanoma CD8+ tumor-infiltrating lymphocyte systems is required.

PMID 42763729
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PubMedDermatology and therapy2026-09-20

The Role of the Microbiome in Lichen Sclerosus: Pathophysiological Insights and Therapeutic Implications.

Kasprowicz-Furmańczyk Marta M, Chmielnicki Witold W, Zdanowska Natalia N, Owczarczyk-Saczonek Agnieszka A

Lichen sclerosus (LS) is a chronic inflammatory and fibrotic dermatosis of unclear etiology, traditionally considered an autoimmune disorder. Emerging evidence suggests that microbiome dysbiosis may contribute to disease pathogenesis by modulating local immune responses and tissue remodeling. This narrative review synthesizes current data on the skin, genital, and gut microbiome in LS, focusing on potential mechanistic links between microbial imbalance and immune activation. Available studies consistently show alterations in microbial composition; however, findings remain heterogeneous because of the small sample sizes, methodological variability, and predominantly cross-sectional designs. Despite these limitations, accumulating data indicate that microbial dysbiosis may influence key immunological pathways involved in LS, including T-cell activation and chronic inflammation. In particular, mucosa-associated invariant T (MAIT) cells are proposed as a potential mechanistic bridge between microbial-derived signals and immune dysregulation, although their role in LS remains unclear. These observations support a conceptual model of LS as a microbiome-modulated inflammatory and fibrotic disorder rather than a purely autoimmune condition. Clinically, microbiome profiling and targeted modulation may offer novel diagnostic and therapeutic opportunities. Future research should prioritize longitudinal and interventional studies, ideally incorporating multi-omics approaches, to clarify causality and facilitate translation into clinical practice.

PMID 42763356
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