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artemisinin (artemisinin, Mateon / ArtiShield / ARTIVeda)

✓ Approved

Oncotelic Therapeutics, Inc. · 治疗药物

什么是 artemisinin？

artemisinin 是一种治疗药物，由Oncotelic Therapeutics, Inc.研发。该药已获批，用于治疗相关适应症，给药途径：Oral (PO)。

药物档案

商品名artemisinin, Mateon, ArtiShield, ARTIVeda
公司Oncotelic Therapeutics, Inc.
给药途径Oral (PO)
状态Approved
来源： ClinicalTrials.gov, Oncotelic Therapeutics, Inc.

治疗适应症

artemisinin 针对 6 个适应症，涉及 6 个治疗领域。

治疗领域疾病/病症分期
InvestigationsBody temperature increased✓ Approved
Hepatobiliary disordersHepatitis✓ Approved
General disorders and administration site conditionsPyrexia✓ Approved
Infections and infestationsCOVID-19Phase I
Respiratory, thoracic and mediastinal disordersAcute respiratory distress syndromePhase I

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相关研究文献

PubMedMalaria journal2026-10-26

Molecular characterization of antimalarial resistance and hrp2/3 deletions in Plasmodium falciparum strains from Mtwara, Tanzania (2021-2024).

Thapradit Piyathida P, Pagornrat Watcharee W, Madmanee Wanassanan W, Sangsri Raweewan R et al.

Malaria remains a significant public health challenge in sub-Saharan Africa and Southeast Asia, with Plasmodium falciparum responsible for the majority of infections and deaths, particularly among children aged < 5 years. In Tanzania, the widespread use of antimalarial drugs, such as sulfadoxine-pyrimethamine for preventive therapy and artemisinin-based combination therapies as first-line treatment, has prompted concerns about the emergence and spread of drug resistance. The prolonged use of these drugs may have influenced resistance patterns, varying over time. Moreover, some P. falciparum samples have been reported as rapid diagnostic test (RDT)-negative despite microscopic confirmation of P. falciparum infection, raising questions about whether such false-negative results are due to poor-quality RDT kits or genetic deletions in the parasite. This study investigated drug resistance dynamics and potential false-negative RDT results in P. falciparum by analyzing molecular markers in pfdhps, pfdhfr, pfkelch13, and pfhrp2/3, with the 18S rRNA gene used as a housekeeping control to verify DNA quality and confirm true parasite positivity. Molecular analysis revealed a decline in the triple pfdhfr mutation paired with double pfdhps mutations, alongside an increase in mixed dhfr-dhps haplotypes (χ2 = 28.94, p < 0.001), indicating ongoing genetic diversification under drug pressure. Wild-type parasites were predominant (56-76%), and most pfkelch13 mutations were located in the non-propeller region, with no validated or candidate mutations associated with artemisinin-resistance detected. P. falciparum-infected samples that were RDT-negative showed a high frequency of both complete and partial deletions in pfhrp2 and pfhrp3, potentially explaining RDT inconsistencies and false-negative results. P. falciparum remains the dominant species in this high-transmission region, showing a persistently high rate of antifolate resistance. Significant associations between triple pfdhfr and double pfdhps resistance markers were observed between 2021 and 2024. The continued susceptibility to artemisinin emphasizes the need for ongoing molecular surveillance and monitoring of hrp2/hrp3 deletions to support malaria control strategies in Tanzania.

PMID 42928299
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PubMedFood research international (Ottawa, Ont.)2026-10-23

Zearalenone promotes hepatic lipid accumulation via EGFR-HSP90 complex stabilization.

Huangfu Bingxin B, Wang Teng T, Li Jie J, Zhao Yijia Y et al.

Zearalenone (ZEA), a widespread foodborne mycotoxin, has been implicated in metabolic dysfunction-associated fatty liver disease (MAFLD), although its direct hepatic targets and mechanisms remain unclear. This study aimed to identify the molecular target of ZEA and elucidate its role in hepatic lipid dysregulation. Using drug affinity responsive target stability, network toxicology, molecular docking, cellular thermal shift assay, microscale thermophoresis, and molecular dynamics simulations, epidermal growth factor receptor (EGFR) was identified as a direct binding target of ZEA. In C57BL/6J mice (0.5 mg/kg·body weight, 5-day oral gavage) and HepG2 cells (0-20 μM ZEA), ZEA activated EGFR signaling by enhancing transcription and stabilizing EGFR protein via promotion of the EGFR-HSP90 complex. EGFR activation promoted proteolytic cleavage and nuclear translocation of SREBP1c, leading to upregulation of lipogenic enzymes (SCD1, ACC, FASN) and exacerbated lipid accumulation, especially under high fatty acid conditions. Artemether (Art), an artemisinin derivative reported to disrupt the EGFR-HSP90 complex and improve hepatic lipid metabolism, was therefore selected as a therapeutic intervention. Art significantly attenuated EGFR expression and downstream lipogenesis by disrupting the EGFR-HSP90 complex, thereby alleviating ZEA-induced lipid deposition. The EGFR inhibitor erlotinib reversed both ZEA-induced lipogenesis and the protective effects of Art, confirming the central role of EGFR signaling. Collectively, ZEA promotes hepatic lipid accumulation via stabilization of the EGFR-HSP90 complex and activation of the EGFR-SREBP1c axis, suggesting EGFR as a potential therapeutic target.

PMID 42914464
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PubMedFrontiers in pharmacology2026-10-20

Antidepressant effects of artemisinin and its derivatives: a systematic review and meta-analysis of randomized controlled animal studies.

Tian Yuan Y, Zhang Haiping H, Zhang Xu X, Wang Luyao L

Depression imposes a substantial global disease burden. Current pharmacotherapies are often limited by a delayed onset of action, significant adverse effects, and high costs. Preclinical studies have indicated that artemisinin and its derivatives possess neuroprotective and anti-inflammatory properties and have demonstrated antidepressant-like effects in rodent models. However, no meta-analysis has yet been performed on these preclinical rodent studies. This study aimed to systematically evaluate the antidepressant efficacy of artemisinin in rodent models of depression-like behavior and to identify potential factors influencing the variability in treatment effects. This study systematically searched four databases (PubMed, Web of Science, Embase, and China National Knowledge Infrastructure), including randomized controlled trials (RCTs) published up to May 2026. All data were statistically analyzed using a random-effects model, yielding standardized mean differences (SMDs) with their 95% confidence intervals (CIs). Subgroup analyses were conducted based on rodent species, depression-like modeling methods, intervention timing, duration, and frequency. Publication bias was assessed using Egger's test, funnel plots, and trim-and-fill analyses. Sensitivity analyses were performed to evaluate result robustness. The risk of bias was evaluated using the Systematic Review Centre for Laboratory Animal Experimentation (SYRCLE) tool, and the overall certainty of evidence was evaluated using the Grading of Recommendations Assessment, Development and Evaluation (GRADE) framework. A total of 17 studies involving 402 rodents were included in the analysis. Compared with the control group, artemisinin reduced immobility in the TST and FST, increased sucrose preference in the SPT, alleviated anxiety-like behaviors in the OFT and EPM, and improved cognitive performance in the MWM, Y-maze, and NOR. Subgroup analyses identified intervention duration, frequency, species, modeling methods, and derivative type as impactful moderators. Sensitivity tests validated stable outcomes. While Egger's test hinted at publication bias in the OFT, TST, and FST datasets, trim-and-fill analyses imputed zero missing studies, although this does not fully exclude publication bias given the limited number of studies. Under the GRADE framework, the certainty of evidence was rated as very low for most outcomes due to high risk of bias, substantial heterogeneity, and indirectness. Artemisinin can ameliorate depression-like and anxiety-like behaviors and improve cognitive function. These findings provide a basis for further investigation into artemisinin as an adjunctive therapeutic agent for depression. However, the certainty of evidence is very low due to methodological limitations in the included preclinical studies, and additional clinical trials are required to evaluate its efficacy in humans.

PMID 42898534
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PubMedThe American journal of tropical medicine and hygiene2026-10-20

Absence of Validated and Candidate Plasmodium falciparum Kelch13 Markers of Artemisinin Resistance and Low Frequency of a Pfcoronin Mutation in Igombe, Mwanza Region, Tanzania.

Marwa Karol J KJ, Oliveira Rafael R, Mwaiswelo Richard O RO, van Loon Welmoed W et al.

Tanzania recently identified partial artemisinin resistance in the Kagera region bordering Rwanda and Uganda, where resistance is established. Monitoring neighboring regions is critical to guide containment strategies. We, therefore, conducted molecular surveillance of Plasmodium falciparum Kelch13 (pfk13) and Plasmodium falciparum actin-binding protein coronin (pfcoronin; P76S) mutations in Igombe in Mwanza region. In a health facility-based cross-sectional study in 2025, P. falciparum DNA from patients with uncomplicated malaria was analyzed using polymerase chain reaction, Sanger sequencing, and allele-specific melting curve assays. Among 121 sequenced isolates, no validated or candidate pfk13 mutations were detected. The nonsynonymous, nonvalidated pfk13 variant N489K occurred in 2.5%. The pfcoronin P76S mutation was observed at low prevalence (3.6%). Despite proximity to Kagera hot spots, validated pfk13 markers have not yet been established in the Mwanza region. The presence of pfcoronin P76S, albeit at low levels, requires careful monitoring. Continued molecular surveillance is essential to support the early detection and containment of emerging artemisinin resistance in Tanzania.

PMID 42901154
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PubMedInfection2026-10-20

Emerging antimalarial drug targets to combat drug-resistant malaria parasites.

Nehra Rohit R, Yadav Urvashi U, Ranjha Ritesh R, Mohan Mradul M et al.

The emergence and rapid spread of multidrug resistance in Plasmodium parasites, particularly in the Greater Mekong region and increasingly in Sub-Saharan Africa. Resistance has led to an urgent need to develop novel anti-malaria therapies with an effective mechanism. Several non-classical targets, including Na++ pump PfATP4 (Plasmodium falciparum ATPase 4), PI4K (Phosphatidylinositol 4-kinase) and PfNCR1(Plasmodium falciparum Niemann-Pick Type C1-Related protein), are highly active against the asexual stage of Plasmodium. We summarise the progress achieved on key emerging targets over past decade and emerging pipeline of artemisinin-combination therapies (ACTs). Other targets, such as dihydroorotate dehydrogenase (PfDHODH) for pyrimidine biosynthesis, ion transporters, mitochondrial electron transport chain, and apicoplast metabolic pathways, have demonstrated significant therapeutic potential due to their essential roles in parasite physiology and minimal homology to human counterparts. Combating drug-resistant malaria parasites and strengthening the global antimalarial drug pipeline for long-term disease control can be achieved by developing new ways to target parasites. This comprehensive review discusses the current status of novel antimalarial drug targets, recent discoveries and future of novel therapies in the following innovation areas: Protein synthesis machinery as drug targets, hemoglobin metabolism targets, transport proteins therapeutic targets, Kinase targets, Organelles and cell targets, and mitochondrial targets, which fill critical gaps in the existing therapeutic arsenal.

PMID 42900459
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PubMedZhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery2026-10-19

[L-lactylation regulatory network in orthopedic degenerative diseases].

Shen Jianlin J, Xu Yiting Y, Yang Jialin J, Xu Miao M et al.

To explore the therapeutic potential of L-lactylation in degenerative disc disease, arthritis, muscle degeneration, exercise metabolism, and osteoporosis. Literatures about L-lactylation in metabolic regulation, inflammatory response, and bone homeostasis at home and abroad in recent years were extensively reviewed. Emphasis was placed on analyzing the molecular regulatory networks of L-lactylation and its related clinical therapeutic potential in intervertebral disc degenerative diseases, arthritis, muscle degeneration and exercise metabolism, and osteoporosis. L-lactylation reprograms metabolic flux by modifying key enzymes, and regulates chromatin dynamics through histone/non-histone modifications, thereby modulating macrophage polarization, osteoclast-osteoblast balance, and extracellular matrix remodeling. In intervertebral disc degeneration, tumor necrosis factor α activates glycolytic enzymes to promote L-lactylation, while glutamine supplementation reduces L-lactylation levels and activates the adenosine monophosphate-activated protein kinase catalytic subunit α pathway; hypoxia inducible factor 1α promotes the extracellular transport of L-lactylation by upregulating monocarboxylate transporter 4. In osteoarthritis, lactate dehydrogenase A (LDHA) overexpression leads to elevated histone L-lactylation levels, which in turn upregulates the transcriptional activity of triosephosphate isomerase 1 and accelerates cartilage degradation. In rheumatoid arthritis, artemisinin induces L-lactylation of pyruvate kinase M2 and inhibits the proliferation and migration of fibroblast-like synoviocytes. In tendinopathy, L-lactylation exerts regulatory effects in the aspects of extracellular matrix, immunity, nerves and blood vessels. In osteoporosis, L-lactylation affects osteogenic differentiation and bone resorption through regulatory axes such as Forkhead box F1, crystallin alpha B/ferritin heavy chain 1, and JunB, and interventions including LDHA regulation and scopolamine administration can promote osteogenic differentiation. L-lactylation plays a dual regulatory role in orthopedic degenerative diseases, and its spatiotemporal dynamics and tissue specificity provide new opportunities for precise treatment. Although target specificity and clinical validation still face challenges, targeting L-lactylation modification is expected to become a new direction for disease-modifying therapy of orthopedic degenerative diseases.

PMID 42897005
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