Drug Database
PO

polio vaccine (OPV, Bio Farma / tOPV, Bio Farma)

✓ Approved

Bio Farma · Vaccine · Vaccine

What is polio vaccine?

polio vaccine is a vaccine developed by Bio Farma. It is approved for therapeutic indications via oral (po).

Drug Profile

Brand NamesOPV, Bio Farma, tOPV, Bio Farma
CompanyBio Farma
Drug ClassVaccine, Large Molecules
RouteOral (PO)
StatusApproved
Sources: ClinicalTrials.gov, Bio Farma

Therapeutic Indications

polio vaccine is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Surgical and medical proceduresPolio immunisation✓ Approved

Related Research Articles

PubMedAdvances in virology2026-09-20

Comparative Sequence Analysis of the Envelope Gene of Kyasanur Forest Disease Virus Vaccine Strain With Currently Circulating Field Strains.

Kaje Keerthi K, Marinaik Chandranaik B CB, Gomes Amitha Reena AR, Rizwan Apsana A et al.

The present study was undertaken with the objective of performing comparative sequence analysis of the envelope (E) gene of Kyasanur forest disease virus (KFDV) vaccine strain P9605 with the circulating field strains. The study was taken up as the currently used KFDV vaccine strain, KFDV P9605, was isolated in the 1960s. For this study, we designed two sets of primers targeting the complete amplification of the E gene of KFDV. The sequencing was performed by the Sanger method, and the deduced sequence of the vaccine virus was deposited in GenBank with accession number PX067005. This sequence obtained for the vaccine virus was aligned and compared with sequences of GenBank-deposited circulating field strains. We also performed comparative sequence analysis of the Kyasanur forest disease (KFD) vaccine seed virus having passaged twice in mouse brain with the vaccine seed virus passaged six times in mouse brain to investigate whether multiple passages in mouse brain will lead to genetic mutation in the immunologically important E gene. The phylogenetic analysis revealed seven amino acid mutations in the field strains at positions A123T, S158N, D178E, D239N, A313S, M429I, and G479A when compared with the vaccine strain. We did not find any mutations at the critical fusogenic segment (residues 98-113) in the E gene of currently circulating field strains compared to the vaccine seed virus. The study found no genetic variations in the E gene of the KFD virus passed two times and passed six times in mouse brain. We performed SWISS-MODEL homology modeling, AlphaFold protein analysis, and Ramachandran plot analysis to study the E protein structures and stability. The observations made in this study suggest slow evolutionary drift and conserved structural stability of the envelope gene of KFDV ever since its emergence 7 decades ago; however, the functional implications of these amino acid substitutions need further studies on their roles in viral infectivity, transmission, and impact on immunity.

PMID 42763584
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PubMedOncoTargets and therapy2026-09-20

Trehalose Exerts Selective Cytotoxicity Against Tongue Squamous Cell Carcinoma Cells While Exhibiting Limited Cytotoxicity Toward Normal Oral Squamous Cells.

Jiao Liang L, Zheng Fuju F, Yu Shuyang S, Zhang Jingfen J et al.

Chemotherapy-induced oral mucositis is a major complication in tongue squamous cell carcinoma (TSCC) treatment, caused by non-selective cytotoxicity of chemotherapeutic agents. Trehalose is a natural disaccharide with reported antitumor and cell-preserving properties, but its selective effect on TSCC versus normal oral cells remains unclear. This study aimed to evaluate whether trehalose exerts differential effects on TSCC cells and normal oral squamous cells (NOSCs). We treated two TSCC cell lines (CAL-27, SCC-15) and normal oral squamous cells (NOSCs) with trehalose at different concentrations. Cell proliferation, apoptosis, migration and invasion were evaluated in vitro. Angiogenesis was assessed using the chick embryo chorioallantoic membrane assay, and in vivo antitumor activity was verified in a nude mouse xenograft model. At 200 mmol/L, trehalose significantly inhibited proliferation, migration and invasion, and induced apoptosis in TSCC cells, while showing comparatively limited cytotoxicity toward NOSCs. Trehalose also reduced angiogenic activity in the CAM assay and decreased tumor growth and was associated with less extensive Ki-67 immunostaining in vivo. IL-1β, IL-6, and TNF-α levels increased after trehalose treatment; these changes were considered treatment-associated responses rather than evidence of a causal mechanism of apoptosis. Trehalose selectively inhibited TSCC cells while showing comparatively limited cytotoxicity toward normal oral cells. These findings support further investigation of trehalose as a potential antitumor candidate, while its possible relevance to chemotherapy-induced oral mucositis requires direct validation in dedicated models.

PMID 42763747
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PubMedBritish journal of cancer2026-09-20

PAX9 activates autophagy through a transcription-dependent mechanism, promoting EGFR degradation to restrict cell survival in oral cancer.

Bhol Chandra Sekhar CS, Kar Rakesh Kumar RK, Mishra Soumya Ranjan SR, Mishra Priyadarshini P et al.

PAX9 (paired box 9) gene, a transcription factor belonging to the PAX family, is associated with craniofacial development. Dysregulation of PAX9 is associated with oral squamous cell carcinoma (OSCC), and its functional regulation in OSCC remains unknown. PAX9 expression was evaluated in human OSCC tissues and a DMBA-induced hamster oral carcinogenesis model, and its functional role in cell death and autophagy was assessed using PAX9 overexpression and PAX9 mutants in OSCC. Autophagy, lysosomal activity, apoptosis, EGFR degradation, and chemosensitivity were analysed in vitro and in an OSCC xenograft model. Overexpression of PAX9 activated autophagy and enhanced lysosomal function through a transcription-dependent mechanism, thereby inducing apoptosis in OSCC. Mutations at L27P and I29T in PAX9 blocked autophagy and restored cell viability in OSCC. Interestingly, PAX9 was shown to activate lethal autophagy, which degrades EGFR, thereby inducing cell death and chemosensitisation in OSCC. Moreover, PAX9 expression decreased in higher-grade human oral cancers and in DMBA-induced hamster oral carcinogenesis, and in vitro exposure to carcinogens reduced PAX9 while increasing DNMT1, suggesting that DNA methylation may regulate PAX9 during oral carcinogenesis. PAX9 activates lethal autophagy, promoting EGFR degradation and apoptosis in OSCC, highlighting its tumour-suppressive potential and therapeutic relevance.

PMID 42763310
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PubMedOdontology2026-09-20

LL-37-based oral antimicrobial therapeutics: translational challenges and future directions-a narrative review.

J Muruganandhan M, Veeraraghavan Vishnu Priya VP, Govindarajan Sujatha S

LL-37 is an antimicrobial peptide involved in antimicrobial defence, inflammatory regulation, tissue repair, and bone regeneration in the oral cavity. Salivary and gingival crevicular fluid LL-37 levels are associated with disease activity and treatment responses. Although there is solid mechanistic and preclinical data on LL-37, research on clinical applications of this remarkable peptide seem to be stalled due to a multitude of factors. The use of LL-37 in clinical practice is affected by proteolytic degradation, cytotoxicity at higher concentrations, microbial tolerance, biofilm protection, rapid salivary clearance, and high production costs. Our review provides a comprehensive update emphasizing the key gaps in LL-37 research and the translational challenges faced by researchers. We also suggest a three-pronged roadmap to future approaches comprising (i) rational peptide engineering and smart nanocarrier-based delivery, (ii) host-directed induction of endogenous LL-37 via vitamin D and short-chain fatty acid pathways, and (iii) standardisation of salivary/gingival crevicular fluid LL-37 as a non-invasive biomarker, aimed at developing LL-37 as a viable diagnostic and therapeutic agent in periodontal disease, dental caries, endodontic infections, oral mucosal disorders, and oral squamous cell carcinoma. Peptide derivatives, nanocarrier-based delivery systems, combination therapy, and vitamin D-mediated induction are being studied to improve its stability and therapeutic activity. LL-37 may have strong applications in oral diagnosis, prevention, and treatment of oral diseases, if the safety, efficacy, and delivery methods are effectively enhanced.

PMID 42763374
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PubMedOdontology2026-09-20

Sleep duration and oral functional impairment: potential involvement of monocyte-related inflammation.

Tani Shigemasa S, Suzuki Yasuyuki Y, Yagi Tsukasa T, Takahashi Atsuhiko A et al.

Non-optimal sleep duration is associated with systemic inflammation and adverse health outcomes, whereas oral functional impairment has been linked to systemic diseases. However, the mechanisms linking sleep and oral function remain unclear. This study examined the association between sleep duration and perceived masticatory difficulties and whether leukocyte-derived inflammatory markers mediated it. This cross-sectional study included 8,252 adults (mean age, 51.1 years; 59.7% men) undergoing routine health checkups between April 2024 and March 2025. Sleep duration was categorized as < 5, 5-6, 6-7, 7-8, and ≥ 8 h. Perceived masticatory difficulties were assessed using a standardized questionnaire. Systemic inflammation was evaluated using white blood cell (WBC) and differential leukocyte counts. Multivariable regression, restricted cubic spline, and mediation analyses were performed. Masticatory difficulties were reported by 733 participants (8.9%). Those sleeping 7-8 h had the lowest odds of masticatory difficulties. Restricted cubic spline analysis demonstrated a significant non-linear association between sleep duration and monocyte levels (P for non-linearity = 0.03), with higher levels at shorter sleep durations and a modest increase at longer durations. Mediation analysis showed a significant indirect effect through monocyte count (indirect effect = - 0.0031; 95% confidence interval, - 0.0072 to - 0.0003), whereas WBC, neutrophil, and lymphocyte counts showed no significant indirect effects. Non-optimal sleep duration was associated with perceived oral functional impairment, partly mediated by monocyte-related inflammation. These findings suggest a potential inflammatory pathway linking sleep and oral function, with monocyte count identified as the sole significant mediator, and support medical-dental collaboration in preventing systemic diseases.

PMID 42763373
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PubMedCureus2026-09-20

Implant-Supported Rehabilitation Following Endodontic Failure in a Patient Classified as American Society of Anesthesiologists (ASA) Physical Status III With Chronic Post-Stroke Hemiplegia: A Multidisciplinary Dental Case Report.

Arenas Perez Nayibe N

Patients with chronic neurological disabilities frequently present significant challenges in dental treatment due to functional limitations, impaired oral hygiene, and concerns regarding medical risk. These challenges often result in delayed care or refusal of treatment, particularly when surgical procedures and implant rehabilitation are required. This report describes the multidisciplinary dental management of a 76-year-old male patient classified as American Society of Anesthesiologists (ASA) Physical Status III with a history of ischemic cerebrovascular accident resulting in chronic right-sided hemiplegia, facial paralysis, wheelchair dependence, and reduced ability to perform oral hygiene independently. The patient presented on an emergency basis with severe pain associated with a previously endodontically treated maxillary right second premolar. Clinical and radiographic evaluation, including cone-beam computed tomography (CBCT), revealed persistent periapical infection consistent with endodontic failure. Given the patient's medical history, a comprehensive hospital-based medical evaluation and neurological clearance were obtained prior to treatment. The patient's poor oral hygiene status was addressed through caregiver-assisted oral hygiene instruction, professional dental cleaning, and infection control measures. Following medical approval, the affected tooth was extracted, and alveolar ridge preservation was performed using particulate bone graft material and a resorbable collagen membrane. After a six-month healing period, implant placement was completed using CBCT-guided treatment planning. Three months later, a definitive screw-retained implant-supported crown was fabricated using a digital workflow and successfully delivered. The patient experienced complete resolution of pain, restoration of masticatory function, and improvement in overall quality of life. This case highlights the importance of multidisciplinary dental management, advanced imaging, medical clearance, and caregiver involvement when treating medically stable ASA III patients with chronic post-stroke disabilities. The outcome observed in this carefully selected patient suggests that implant-supported rehabilitation may be successfully performed when appropriate individualized medical assessment, maintenance, and long-term oral hygiene support are available.

PMID 42763609
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