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aciclovir (aciclovir, Lauriad / Sitavig / BA021)

✓ Approved

Innocutis · · 小分子

什么是 aciclovir？

aciclovir 是一种小分子，由Innocutis研发。该药已获批，用于治疗相关适应症，给药途径：Oral (PO)、Topical。

药物档案

商品名aciclovir, Lauriad, Sitavig, BA021
公司Innocutis
药物类别小分子
给药途径Oral (PO), Topical
状态Approved
来源： ClinicalTrials.gov, Innocutis

作用机制

分子靶点

aciclovir 作用于 1 个分子靶点：

(UL30)
需要更深入的分析？Noah AI 可解释复杂机制并与同类药物比较。

治疗适应症

aciclovir 针对 1 个适应症，涉及 1 个治疗领域。

治疗领域疾病/病症分期
Congenital, familial and genetic disordersCongenital herpes simplex infection✓ Approved

相关研究文献

PubMedOphthalmology and therapy2026-10-23

Aqueous and Vitreous Ketorolac Levels in Combined Cataract and Pars Plana Vitrectomy with Intracameral Ketorolac 0.3% Versus Topical Ketorolac 0.4.

Donnenfeld Eric D ED, Narain Sahas S, Shoshany Talia T, Perry Henry D HD et al.

Ketorolac is well documented to reduce postoperative inflammation, pain, and the risk of cystoid macular edema (CME) during cataract surgery. The concentration of ketorolac in the vitreous humor following topical administration has been reported to be very low. As there is a lack of evidence on the vitreous levels of ketorolac following intracameral administration, this study aimed to evaluate the concentration of ketorolac in aqueous and vitreous humor samples during combined cataract surgery and pars plana vitrectomy in patients receiving preoperative topical ketorolac 0.4% or intracameral phenylephrine 1.0%/ketorolac 0.3% (OMIDRIA®, Rayner Surgical Inc., Bellevue, WA, USA). This prospective, randomized, controlled study recruited patients undergoing combined cataract surgery and pars plana vitrectomy and randomized in a 1:1 ratio to receive either intracameral phenylephrine 1.0%/ketorolac 0.3% (study arm) or preoperative topical ketorolac 0.4% (control arm). Aqueous samples were collected at the start of cataract surgery in the control arm and at the end of cataract surgery in the study arm. The vitreous samples were taken at the start of vitrectomy in all eyes. The samples were frozen and sent to an independent lab (Emery Pharma, Alameda, CA) for analysis. Ketorolac levels were determined using liquid chromatography-tandem mass spectrometry. Five eyes of five patients received ketorolac intracamerally, and six eyes of six patients received it topically. The mean aqueous ketorolac concentration was significantly higher in the study eyes than in the control (20,868.2 ± 7342.4 ng/mL versus 635.1 ± 909.6 ng/mL, p < 0.0001). In the vitreous, the mean ketorolac concentration was significantly higher in the study eyes than in the control (2508.8 ± 4477.6 ng/mL versus 3.1 ± 7.7 ng/mL, p = 0.0004). The intracameral administration of phenylephrine/ketorolac resulted in 33 times higher ketorolac concentration in the aqueous and 809 times higher in the vitreous humor than the topically administered ketorolac during combined cataract surgery and pars plana vitrectomy. ClinicalTrials.gov identifier, NCT06539637, date of registration 29 July 2024 (retrospectively registered).

PMID 42911532
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PubMedFrontiers in endocrinology2026-10-23

Association of clonal hematopoiesis of indeterminate potential with cardiovascular mortality in cardiovascular-kidney-metabolic syndrome: a large prospective cohort study.

Zhao Zehao Z, Ma Changsheng C, Zhao Libo L, Zhao Xiliang X et al.

Cardiovascular-kidney-metabolic (CKM) syndrome represents a progressive pathophysiological continuum. While clonal hematopoiesis of indeterminate potential (CHIP) is known to increase the risk of CKM disease onset and adverse prognoses, its overall and stage-specific impacts on cardiovascular mortality within the CKM framework, alongside the circulating proteomic mechanisms mediating this excess risk, remain largely unknown. Participants from the UK Biobank with available CHIP data across the CKM syndrome continuum were included. The primary outcome was cardiovascular mortality. Kaplan-Meier curves and multivariable Cox proportional hazards models were utilized to evaluate the incremental risk conferred by CHIP. Sensitivity and subgroup analyses were conducted to ascertain result robustness. Within UKB Pharma Proteomics Project (UKB-PPP), circulating proteins jointly associated with CHIP and cardiovascular mortality were identified, followed by functional enrichment and mediation analyses to elucidate the underlying mechanisms. During a median follow-up of 16.5 years, 6,515 cardiovascular deaths were recorded among 288,384 participants across CKM stages 1-4. Across all varying CKM stages, individuals harboring Large CHIP exhibited a significantly higher risk of cardiovascular mortality compared to the non-CHIP group (all log-rank P < 0.05). Following multivariable adjustment, Large CHIP emerged as an independent risk factor for cardiovascular mortality (hazard ratio, 1.24; 95% confidence interval, 1.09-1.40), with subgroup analyses confirming consistent effects regardless of CKM stage or established cardiometabolic and renal diseases. Proteomic profiling, corroborated by UKB-PPP, revealed that the mechanisms driving this excess risk predominantly involve immune-inflammatory dysregulation and tissue structural remodeling. This pathway was highlighted by critical downstream mediators, including the structural component DSC2 (mediating 34.3% of the risk) and key immune-regulatory receptors such as VSIG4 (33.1%) and CD300C (29.2%). CHIP is an independent risk factor for cardiovascular mortality across all stages of CKM syndrome. Mechanistically, CHIP exacerbates this adverse outcome primarily by driving systemic inflammation, immune dysregulation, and aberrant tissue remodeling.

PMID 42909319
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PubMedThe New England journal of medicine2026-10-22

Ianalumab for the Treatment of Patients with Sjögren's Disease.

Mariette Xavier X, Grader-Beck Thomas T, Finzel Stephanie S, Schiopu Elena E et al.

Sjögren's disease is a complex, systemic autoimmune disease with no approved targeted therapies. Ianalumab is an IgG1 monoclonal antibody with a dual mechanism of action, depleting B cells through antibody-dependent cellular cytotoxicity and inhibiting B-cell activation and survival through blockade of B-cell activating factor receptor. We conducted two 52-week, double-blind, randomized, placebo-controlled trials involving patients with active Sjögren's disease. Patients in the NEPTUNUS-1 trial were assigned in a 1:1 ratio to receive subcutaneous ianalumab (300 mg monthly) or placebo; patients in the NEPTUNUS-2 trial were assigned in a 1:1:1 ratio to receive 300 mg of ianalumab monthly or every 3 months or placebo. The primary end point was the change from baseline in the score on the European Alliance of Associations for Rheumatology (EULAR) Sjögren's Syndrome Disease Activity Index (ESSDAI) at week 48 (scores range from 0 to 123, with higher scores indicating greater disease activity). The first key secondary end point in the hierarchical plan for the NEPTUNUS-1 trial was an ESSDAI response (≥5-point reduction) at week 48; for the NEPTUNUS-2 trial, it was the change from baseline in the score on the Sjögren's Syndrome Symptom Diary (SSSD) or EULAR Sjögren's Syndrome Patient Reported Index (ESSPRI) at week 48. Overall, 275 patients underwent randomization in the NEPTUNUS-1 trial (ianalumab monthly, 137 patients; placebo, 138 patients) and 504 in the NEPTUNUS-2 trial (ianalumab monthly, 168 patients; ianalumab every 3 months, 167 patients; and placebo, 169 patients). In both trials, ianalumab monthly led to a significantly greater decrease in the ESSDAI score at week 48 than placebo, with a between-group difference of -1.3 points (95% confidence interval [CI], -2.6 to 0.0; P = 0.0496) in NEPTUNUS-1 and -1.0 points (95% CI, -2.0 to 0.0; P = 0.04) in NEPTUNUS-2. No significant differences in the incidence of an ESSDAI response or in the change from baseline in SSSD or ESSPRI scores were observed at week 48. The incidence of serious adverse events was similar with ianalumab and placebo. Nonserious local injection-site and systemic injection-related reactions were more common in the ianalumab groups. In these two trials involving patients with active Sjögren's disease, ianalumab at a dose of 300 mg monthly resulted in a significantly greater decrease in disease activity at week 48 than placebo, although there were no significant differences in the incidence of an ESSDAI response or in the change from baseline in SSSD or ESSPRI symptom scores. (Funded by Novartis Pharma; NEPTUNUS-1 and NEPTUNUS-2 ClinicalTrials.gov numbers, NCT05350072 and NCT05349214, respectively.).

PMID 42906087
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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.

PMID 42894645
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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.

PMID 42895254
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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.

PMID 42889699
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