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TU

tuberculosis vaccine

✓ Approved

SK Chemicals · Cell-based Therapies · Cell-based Therapies

What is tuberculosis vaccine?

tuberculosis vaccine is a cell-based therapies developed by SK Chemicals. It is approved for therapeutic indications via injectable (others) or intradermal injection.

Drug Profile

CompanySK Chemicals
Drug ClassCell-based Therapies, Vaccine
RouteInjectable (Others), Intradermal Injection
StatusApproved
Sources: ClinicalTrials.gov, SK Chemicals

Related Research Articles

PubMedbioRxiv : the preprint server for biology2026-07-17

Enhancement of a STING Agonist Vaccine for Tuberculosis Using Locally Supercharged MS2 Viral Capsids.

Martin Hannah S HS, Lamb-Echegaray Isabel D ID, Huang Paul P, Shallow Lillian L et al.

Mycobacterium tuberculosis (Mtb) infection kills more people worldwide than any other pathogen. While the Bacille Calmette-Guérin (BCG) vaccine for Mtb has been widely used for over a century, it provides insufficient protection to eradicate this disease. One of our labs has recently established that a protein antigen (H1) can be combined with a STING pathway agonist to achieve strong protection against Mtb in mice, with performance that exceeds that of the BCG vaccine. However, its reliance on a synthetic cyclic dinucleotide (CDN) with relatively poor cell uptake requires higher dosing levels, thus increasing costs. To increase the efficiency of this vaccine and provide a delivery strategy that could also be used in humans, the H1 Mtb antigen and CDN adjuvant were conjugated to genome-free MS2 viral capsids that included cationic mutations to increase cell uptake. Specifically, the H1 antigen was conjugated to the external surface of MS2 using a tyrosinase-mediated oxidative coupling reaction, and the native STING agonist cGAMP was coupled to internal cysteine residues through a reductively cleavable disulfide linker. The resulting MS2-H1 and MS2-cGAMP conjugates were then co-delivered for three doses of vaccination in mice before exposure to Mtb. The MS2-based vaccine platform was observed to have comparable efficacy to the original H1/CDN formulation, but its enhanced uptake properties enabled 57-fold less CDN and 3-fold less H1 antigen. Additionally, this vaccine elicited immune responses that have been previously demonstrated to correlate with protection. The ability of the capsid shells to protect the CDN cargo during transport allowed enzymatically produced, and thus readily accessible, cGAMP to be used instead of more costly CDNs that require many synthetic steps. This, combined with the reduced overall amount of CDN and H1 that was required, could lower the production costs of future vaccines substantially. Finally, the ability of the capsid-based carriers to bypass the membrane transporters for CDNs suggests that this enhanced vaccination platform is likely to exhibit improved human efficacy in future studies.

PMID 42465257
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PubMedThe Journal of biological chemistry2026-07-17

Engineering internally His-tagged ESX secretion system fusion antigens for tuberculosis nanoparticle vaccines.

Hsu Wen-Ling WL, Jiao Yang Y, Huang Wei-Chiao WC, Tran Kristina N KN et al.

Improved tuberculosis (TB) vaccines are needed to combat the disease, a leading cause of infectious disease death worldwide. The culture filtrate TB antigens ESAT6 and CFP10 form dimeric complexes, serve as immune markers for TB exposure and are vaccine antigen candidates. Here, we report that expressing an ESAT6-CFP10 fusion protein with a conventional glycine-serine linker sequence significantly enhanced expression yield in E. coli compared to the single antigens. Substituting an internal His-tag generated the ESAT(Int7)CFP fusion, retained elevated expression levels while simultaneously enabled purification with immobilized metal chromatography. The internal His-tag also permitted rapid protein coupling with cobalt-porphyrin (CoPoP) liposomes. Immunization with these constructs elicited antigen-specific antibodies and T cell responses and reduced lung bacterial burden in mice following aerosol TB challenge. Another pair of TB culture filtrate antigens, EsxH and EsxG yielded no soluble protein as individual antigens. However, when linked with an internal His-tag, high soluble expression was observed for EsxH(Int7)EsxG, and this fusion antigen also conferred protective immunity in TB challenged mice after vaccination with CoPoP. These findings support the design and manufacturability of multivalent TB vaccine candidates through engineered fusion antigens and nanoparticle delivery platforms.

PMID 42463054
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PubMedFrontiers in immunology2026-07-17

Molecular signaling in coinfection: how M. tuberculosis and respiratory viruses rewire host immunity and alter TB outcomes.

Feya Qaqamba Q, Mkhize-Kwitshana Zilungile Lynette ZL, Milase Ridwaan Nazeer RN, Wadee Ahmed A et al.

Tuberculosis (TB) caused by Mycobacterium tuberculosis (M. tuberculosis) and respiratory viral infections remain major, intersecting global health challenges, and their co-occurrence imposes a disproportionate burden in high-HIV/high-TB regions such as sub-Saharan Africa. Coinfection biology is heterogeneous and dynamic, driven by viral diversity including severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), influenza A/B, Respiratory Syncytial Virus (RSV), parainfluenza, metapneumovirus, rhinovirus, adenovirus, and bocavirus, and by the underlying TB stage, from latent and subclinical to active and reactivation disease. Innate sensing pathways, such as Toll-like receptors (TLR), retinoic acid-inducible gene I (RIG-I), and cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING), converge during coinfection, reshaping type I interferon (IFN-I), Nuclear Factor kappa-light-chain-enhancer of activated B cells (NF-κB), and AP-1-driven responses and triggering a network of autocrine and paracrine signaling that reprograms macrophages, dendritic cells, and T-cell subsets. This immune rewiring alters granuloma equilibrium through suppressed Th1/IFN-γ coordination, exaggerated Th17/IL-17-driven neutrophilia, and regulatory T-cell or IL-10-mediated dampening, which together destabilize macrophage activation and tissue architecture. Oxidative stress, mitochondrial dysfunction, and Matrix Metalloproteinases (MMP)-driven matrix remodeling further integrate with these pathways, converting inflammatory signals into epithelial damage, cavitation, and fibrosis. Consequently, disease outcomes depend critically on timing, viral burden, pathogen order, host immune endotype, and TB stage, such that the same virus can either preserve containment or drive progression depending on the local immunological context. Importantly, the effects of respiratory viral coinfection vary across the TB disease continuum, influencing early granuloma formation, latent infection, reactivation risk, and established disease through distinct immunological mechanisms. Host-directed therapies (HDT) targeting interferon, IL-1, TNF, inflammasome, or metabolic checkpoints hold mechanistic promise but exhibit variable clinical translation, underscoring the need for precision approaches that integrate stage- and endotype-specific biomarkers. This narrative review proposes an integrated systems framework that links viral sensing, immune rewiring, granuloma biology, and tissue-remodeling to TB-respiratory virus coinfection, and emphasizes how timing-aware, biomarker-guided strategies can refine diagnosis, clinical management, prognosis, and vaccine design in vulnerable populations.

PMID 42465772
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PubMedFrontiers in cellular and infection microbiology2026-07-17

Application of metagenomic next-generation sequencing in HIV-negative hematogenous disseminated tuberculosis.

Luo Lingxin L, Zhan Jvrong J, Wang Zhen Z, Du Xianzhi X et al.

Hematogenous disseminated tuberculosis (Hematogenous disseminated tuberculosis, HDTB) is a rare, critical form of tuberculosis with a high case fatality ratio and is uncommon in HIV-negative patients. Early recognition of this disease is difficult, and limitations of traditional testing methods often lead to delayed diagnosis. This study aims to investigate the value of metagenomic Next-Generation Sequencing (metagenomic Next-Generation Sequencing, mNGS), as a promising tool, in the diagnosis of hematogenous disseminated tuberculosis in HIV-negative (Human Immunodeficiency Virus, HIV) patients. A retrospective analysis was conducted of the clinical data of 10 HIV-negative patients with hematogenous disseminated tuberculosis confirmed by mNGS. All patients had pre-existing diseases that could lead to impaired immune function. Common symptoms included hyperpyrexia, cough, and dyspnea, and 6 patients developed respiratory failure. C-reactive protein (C-reactive protein, CRP) and procalcitonin (procalcitonin, PCT) levels were both elevated, and PCT was markedly elevated in more than half of the patients, using 0.5 ng/mL as the cutoff value. Most patients had markedly elevated D-dimer levels accompanied by thrombotic events, including 3 patients with concomitant pulmonary embolism. Chest imaging showed patchy pulmonary opacities, and 2 patients had atypical bilateral pleural effusion; these nonspecific findings were easily confused with those of other diseases. Blood mNGS detected Mycobacterium tuberculosis within 2 to 3 days. According to the presence or absence of concomitant pulmonary tuberculosis, the patients were divided into the pulmonary tuberculosis subgroup (pulmonary tuberculosis subgroup, PTB) and the non-pulmonary tuberculosis subgroup (non-pulmonary tuberculosis subgroup, non-PTB). The oxygenation index was significantly lower in the pulmonary tuberculosis subgroup than in the non-pulmonary tuberculosis subgroup (P = 0.037). All cases of pulmonary embolism occurred in the pulmonary tuberculosis subgroup, but the difference was not statistically significant. HIV-negative patients with hematogenously disseminated tuberculosis have atypical clinical manifestations and are prone to incorrect diagnosis. The application of mNGS helps shorten diagnostic delays and accelerate disease control, providing an effective supplementary diagnostic pathway when conventional testing methods cannot identify the pathogen.

PMID 42465845
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PubMedEuropean journal of case reports in internal medicine2026-07-17

A 24-Year-Old Man with Disseminated Tuberculosis and A Corticosteroid-Refractory Paradoxical Reaction to Anti-Tuberculous Treatment.

Charalampidis Charalampos C, Karantana Valentina V, Kavatha Dimitra D, Tsiodras Sotirios S et al.

Paradoxical reactions during anti-tuberculosis treatment are immune-mediated reactions that complicate treatment even in immunocompetent patients. We present the case of a previously healthy 24-year-old man with disseminated tuberculosis, who experienced persistent fever, weight loss, and radiological deterioration despite appropriate treatment. These findings were consistent with a paradoxical reaction to treatment, after extensive work-up excluded treatment failure, co-infections, and systemic inflammatory conditions. However, high-dose corticosteroids failed to achieve improvement. Ultimately, an interleukin-1 receptor antagonist (anakinra) was initiated as a salvage therapy for this corticosteroid-refractory paradoxical reaction, resulting in rapid defervescence, normalization of inflammatory markers, and radiological improvement. This case underscores the diagnostic and therapeutic challenges when managing severe reactions in tuberculosis patients, while highlighting the importance of biologics like anakinra in corticosteroid-refractory paradoxical reactions. Paradoxical reactions to anti-tuberculosis treatment remain an overlooked cause of non-resolving fever in immunocompetent and immunocompromised patients with tuberculosis and should be considered after ruling out treatment-refractory or complicated infection in persistently febrile patients.Prompt treatment of severe reactions prevents major complications and improves clinical outcomes.Corticosteroid-refractory paradoxical reactions illustrate the potential role of biologics, such as tumour necrosis factor inhibitors and, in our case, interleukin-1 receptor antagonists, in controlling excessive inflammation in tuberculosis.

PMID 42466226
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PubMedClinical infectious diseases : an official publication of the Infectious Diseases Society of America2026-07-17

Artificial Intelligence Across the Vaccine Clinical Trial Lifecycle: Evidence, Readiness, and Guardrails.

Idriss Jad J, Kalash Suha S, Faraj Jana Abu JA, Nolan Lauren L et al.

Artificial intelligence (AI) is increasingly being used to support clinical research, but its value in vaccine clinical trials requires careful evidence-based assessment. Vaccine trials pose distinctive challenges, including high safety expectations in healthy participants, evolving pathogen exposure and baseline immunity, incomplete correlates of protection, applicability of findings to intended-use populations, and intense public scrutiny. We conducted a structured, vaccine-focused narrative review of AI applications across the vaccine trial lifecycle, supplemented by targeted clinical trial and vaccine pharmacovigilance studies with directly transferable methods. In the combined evidence base, evidence is strongest for operational uses, particularly recruitment, eligibility screening, trial matching, and risk-based monitoring. Applications to immune-response interpretation, correlates of protection, and vaccine safety surveillance are promising but remain less prospectively validated. Responsible adoption should be guided by intended tool use, evidence of strength, data governance, regulatory expectations, and preservation of human scientific and safety judgment.

PMID 42464875
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