Drug Database
AC

aciclovir (aciclovir, Lauriad / Sitavig / BA021)

✓ Approved

Innocutis · · Small Molecule

What is aciclovir?

aciclovir is a small molecule developed by Innocutis. It is approved for therapeutic indications via oral (po) or topical.

Drug Profile

Brand Namesaciclovir, Lauriad, Sitavig, BA021
CompanyInnocutis
Drug ClassSmall Molecule
RouteOral (PO), Topical
StatusApproved
Sources: ClinicalTrials.gov, Innocutis

Mechanism of Action

Molecular Targets

aciclovir acts on 1 molecular target:

(UL30)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

aciclovir is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Congenital, familial and genetic disordersCongenital herpes simplex infection✓ Approved

Related Research Articles

PubMediScience2026-10-19

Plasma proteomic analysis identified potential therapeutic targets for pulmonary arterial hypertension.

Hu Song S, Xie Yuqi Y, Tan Jiang-Shan JS, Guo Ting-Ting TT et al.

Pulmonary arterial hypertension (PAH) remains a progressive disease with high mortality. By integrating the UK Biobank Pharma Proteomics Project (49,272 participants, 337 incident cases) with drug-target Mendelian randomization, we identified 398 plasma proteins associated with incident PAH and 19 with potential causal relevance, 15 of which are druggable. Then we prioritized 5 candidates for expression validation in the Sugen5416 and hypoxia rat model and confirmed significant upregulation of TNFRSF10A and downregulation of UMOD in lung tissue, consistent with human plasma proteomic trends. Subsequent in vitro functional assays demonstrated that UMOD treatment attenuates PAH-related cellular phenotypes, whereas TNFRSF10A knockdown exacerbates pro-pathogenic progression. These results suggest UMOD as a promising protective therapeutic candidate and indicate the inherent complexity of the TNFRSF10A signaling. This integrative study provides a robust framework for translational research, future studies are warranted to elucidate downstream molecular mechanisms and further evaluate the therapeutic efficacy of these candidates.

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PubMedJournal of global health2026-10-19

Large-scale plasma proteomic profiling enhances prediction of heart failure among hypertensive individuals: prospective insights from the UK Biobank.

Li Maohua M, He Xiao X, Xiao Shasha S, Wang Jixiang J et al.

Hypertension is a major risk factor for heart failure (HF), but current clinical models have limited ability to identify high-risk individuals before overt disease. Plasma proteomics may capture early molecular changes and improve risk prediction. We analysed 16,128 hypertensive UK Biobank Pharma Proteomics Project participants without baseline HF. Plasma levels of 2,911 proteins were measured using the Olink Explore platform. Participants were randomly split 1:1 into training and validation sets. HF-associated proteins were identified using Cox models in the training set, followed by LASSO regression to construct a protein risk score (PRS). Model performance was assessed in the validation set using Harrell's C-index, time-dependent ROC analysis, Net Reclassification Improvement (NRI), Integrated Discrimination Improvement (IDI), calibration, and bootstrap validation. A parsimonious panel was derived using LightGBM and sequential forward feature selection. During a median follow-up of 15.1 years, 1,074 participants developed HF. In the training set, 534 proteins were associated with HF after adjustment for demographic and clinical risk factors and were enriched in cytokine signalling, extracellular matrix organisation, and immune-cell migration pathways. The 101-protein PRS was independently associated with incident HF. In the validation set, adding the PRS increased the C-index from 0.670 to 0.786 beyond age and sex, and from 0.727 to 0.787 beyond the Pooled Cohort Equations to Prevent Heart Failure (PCP-HF) model, with improved reclassification and discrimination. PRS levels were elevated years before HF diagnosis. A six-protein panel comprising NT-proBNP, GDF15, BCAN, WFDC2, CTHRC1, and CNTN5 achieved an AUC of 0.775, outperforming NT-proBNP alone. Plasma proteomic profiling improves HF risk prediction among hypertensive individuals beyond conventional clinical factors and may support earlier risk stratification and precision prevention.

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PubMedFrontiers in toxicology2026-10-17

Xeno-free production of lentiviral particles: implementing hPL as FBS replacement in cell culture.

Guedes Mariana Soares MS, Cole Marnie M, Yildiz Daniela D

Commonly used for delivering fluorescent or bioluminescent reporters to target genes, lentiviral vectors are an "easy-to-clone" vehicle to study up- and downregulation of gene expression induced by drug inhibitors, cytokine stimulants, chemicals, and environmental toxicants. To produce viral particles safely, several plasmid constructs are delivered to human embryonic kidney cells (HEK293-T), which use the cellular machinery to package and assemble non-replicative lentiviruses with high efficiency. However, the cell culture of HEK293-T cells still largely relies on the use of fetal bovine serum for cell survival and proliferation. At large scale, this cell culture practice consumes a great amount of animal-derived serum, driving the need for continuous farming of animals whose fetuses would be used to obtain serum, posing grave ethical and practical concerns for human-relevant research. In this study, we present a feasible and scalable method to adapt the culture medium formulation for HEK293-T cells and demonstrate how virus production responds to this cell culture adaptation. Using a commercially available platelet-based supplement derived from human blood byproducts, we maintain cell viability and proliferation rates, with up to 82% confluence, and can produce lentiviruses (approximately 106 infectious units/mL with up to 20% infectivity), while sparing the killing of bovine fetuses for serum collection, in a cost-efficient and humanized manner. Envisioning adoption in the pharma industry and large-scale virus production facilities, this simple yet robust cell medium formulation presents itself as an ethical and practical avenue to advance scientific innovation and bring one more layer of human relevance to biomedical research.

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PubMedMedicine2026-10-17

PLCG1 regulates pyroptosis to inhibit the progression of non-small cell lung cancer: A Mendelian randomization study.

Zhang Yihui Y, Wang Guihui G, Qin Ziwen Z, Mo Ziyan Z et al.

Pyroptosis, an inflammatory form of programmed cell death, has been implicated in non-small cell lung cancer (NSCLC) progression. However, the specific pyroptosis-related genes causally linked to NSCLC and their upstream regulatory mechanisms remain poorly understood. We performed a two-sample Mendelian randomization (MR) study to assess causal relationships between 33 pyroptosis-related genes and NSCLC risk using genetic instruments from the deCODE database and outcome data from the FinnGen consortium (6446 NSCLC cases, 378,749 controls). Inverse-variance weighting was the primary analysis method, with MR-Egger, weighted median, and MR-PRESSO as sensitivity analyses. To identify upstream regulators, we integrated pQTL data from the The UK Biobank Pharma Proteomics Project and performed two-step MR mediation analysis. Identified genes were further validated using mRNA expression data from The Cancer Genome Atlas (TCGA) and genotype-tissue expression (GTEx) databases. MR analysis identified 2 pyroptosis-related genes significantly associated with NSCLC: IL1B (odds ratio [OR] = 1.087, 95% confidence interval [CI] = 1.009-1.171, P = .028) and PLCG1 (OR = 0.874, 95% CI = 0.766-0.997, P = .044). Upstream analysis revealed that AMBP and CCNE1 were causally associated with PLCG1 expression. Mediation analysis demonstrated that PLCG1 mediated 11.7% of the total effect of AMBP on NSCLC risk (mediation effect: OR = 1.02, 95% CI = 1.01-1.03, P = .008). mRNA expression validation confirmed that AMBP and PLCG1 were significantly upregulated in NSCLC tissues compared to normal tissues (P < .001). This study establishes causal links between pyroptosis-related genes and NSCLC, identifying IL1B as a risk factor and PLCG1 as a protective factor. We further demonstrate that AMBP may promote NSCLC progression partly through upregulating PLCG1 expression, with PLCG1 mediating 11.7% of this effect. These findings provide novel insights into pyroptosis regulation in NSCLC and highlight potential therapeutic targets.

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PubMedEClinicalMedicine2026-10-17

Cost-effectiveness of adding enzalutamide vs standard non-steroidal antiandrogen drugs for patients with metastatic hormone-sensitive prostate cancer undergoing standard first-line therapy: a within-trial, secondary end-point analysis of the ENZAMET phase 3, international randomized trial (ANZUP 1304).

Law Chi Kin CK, Stockler Martin R MR, Martin Andrew J AJ, Davis Ian D ID et al.

The ENZAMET randomized trial demonstrated adding enzalutamide to testosterone suppression, compared with a less potent comparator, significantly improved overall and progression-free survival in men with metastatic hormone-sensitive prostate cancer (mHSPC). This study evaluated cost-effectiveness of adding enzalutamide to standard therapy over 60 months. A within-trial cost-effectiveness analysis was conducted from an Australian health system perspective using prospectively collected, observed data from ENZAMET open-label, phase 3 RCT. This study is registered with ClinicalTrials.gov, NCT02446405, ANZCTR, ACTRN12614000110684, and EudraCT, 2014-003190-42. The analysis was conducted utilizing a data cut-off date of January 19, 2022, with a median follow-up of 68 months. Information on disease status, healthcare utilization, and health-related quality of life were extracted from trial records, linked Medicare claims and patient questionnaires. Costs were calculated in 2023 Australian dollars. EQ-5D-5L scores were converted to health utilities using a validated algorithm. Quality-adjusted life years (QALYs) were estimated by multiplying mean health utility with corresponding life-years accumulated. Deterministic and probabilistic sensitivity analyses examined the effect of varying unit price of study drugs, per diem rates of hospital stays, benefits paid from Medicare claims, and health utility values on robustness of results. Data were assessed for missingness and imputation applied where relevant. Enzalutamide was associated with an additional AUD$127,262 per patient in healthcare costs, 0.24 life-years and 0.15 QALYs gained in the first 5 years, compared with non-steroidal antiandrogen therapy. The incremental cost-effectiveness ratio, (ICER) was AUD$543,880 per life-year gained and AUD$835,580 per QALY gained. Results were sensitive to the cost of study drug, with a purchase price of AUD$6.73 per tablet yielding an ICER that met the willingness-to-pay threshold of AUD$50,000 per QALY gained. Of note, hospitalizations were slightly higher in the enzalutamide group; as was use of musculoskeletal medicines, the latter indicating falls and fractures. Although Enzalutamide improves quality-adjusted survival for men with mHSPC, it is unlikely to be cost-effective. Long-term bone health management in survivors is an important clinical consideration. Astellas Pharma and Australian National Health and Medical Research Council.

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PubMedEngineering biology2026-10-15

Building Capacity for the Engineering of Biology and Biomanufacturing in Finland.

Jäntti Jussi J, Penttilä Merja M

Finland's efforts on engineering biology (synthetic biology) originate from the investments in genetic engineering at the beginning of 1980s. The efforts were linked early on with industry, such as dairy companies, vaccine production and production of ethanol and industrial enzymes, and development of commercial scale bioprocesses. Timely support for activities in metabolic engineering, systems biology and genome wide technologies (omics) and incorporating bioinformatics and cell level modelling evolved the field naturally towards synthetic biology and biofoundry activities. This foundation has created a strong basis in industrial biotechnology in particular, its insights and capabilities being increasingly relevant today within the green transition and bioeconomy contexts. In Finland, more than 830 companies are categorised to operate in biotechnology, collectively producing a turnover of 7.1 billion euros and providing jobs for around 19,400 people. Technology and business opportunities are developing fastest in the field of modern biotechnology rooted in molecular biology. Consequently, in the past 15 years, Finland has evidenced the founding of many new biotechnology firms. In relation to bioeconomy, Finland has also a significant research tradition in plant biotechnology and breeding and in pilot scale cultivation of plant cells. Furthermore, engineering biology activities within medical biotechnology and diagnostics are strong. According to a recent report, 88.5% of the revenue of Finnish biotechnology companies comes from activities classified as industrial biotechnology. This article focuses on engineering/synthetic biology developments for industrial biotechnology, including microbial production of food components and pharma products.

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