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artesunate (artesunate, Amivas)

✓ Approved

Amivas · 小分子 · 小分子

什么是 artesunate？

artesunate 是一种小分子，由Amivas研发。该药已获批，用于治疗相关适应症，给药途径：Injectable (Others)、Intravenous (IV)。

药物档案

商品名artesunate, Amivas
公司Amivas
药物类别小分子
给药途径Injectable (Others), Intravenous (IV)
状态Approved
来源： ClinicalTrials.gov, Amivas

治疗适应症

artesunate 针对 2 个适应症，涉及 1 个治疗领域。

治疗领域疾病/病症分期
Infections and infestationsPlasmodium malariae infection✓ Approved
Infections and infestationsCytomegalovirus infectionPreclinical

相关研究文献

PubMedJournal of immunology research2026-08-06

Artesunate Alleviates Inflammatory Injury in Neonatal Acute Respiratory Distress Syndrome Through CCL5-Mediated Pyroptosis of M2 Macrophage Subsets.

Ma Hai-Ran HR, Xie Yan-Mei YM, Zhang Yu-Xuan YX, Cui Chong-He CH et al.

Neonatal acute respiratory distress syndrome (NARDS) is a life-threatening respiratory disorder characterized by high mortality and significant long-term morbidity. Increasing evidence suggests that pyroptosis contributes to pulmonary tissue injury in ARDS. In this study, single-cell RNA sequencing (scRNA-seq) was utilized to investigate the molecular mechanisms underlying pyroptosis within the NARDS microenvironment. Our analysis identified chemokine (C-C motif) ligand (CCL5) expression in M2 macrophages as a potential regulator of pyroptosis associated with impaired tissue repair. Mechanistically, CCL5 was linked to the activation of the pyroptotic pathway through interactions with inflammasome components, promoting caspase-11-dependent gasdermin D (GSDMD) cleavage and interleukin-1β (IL-1β) release. Network pharmacology analysis identified artesunate, a clinically approved antimalarial drug, as a potential inhibitor of CCL5 expression in patients with NARDS. Functional validation showed that artesunate attenuated M2 macrophage pyroptosis, reduced pulmonary injury, and promoted tissue repair. Collectively, our findings identify CCL5 as a potential regulator of macrophage pyroptosis and support the therapeutic potential of artesunate for modulating pyroptosis-associated inflammation in NARDS. This study provides a mechanistic framework for the development of CCL5-targeted interventions and highlights the dual anti-inflammatory and pro-repair properties of artesunate in NARDS treatment.

PMID 42557887
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PubMedThe Journal of the Association of Physicians of India2026-08-03

Artesunate-resistant Plasmodium falciparum at a Tertiary Care Hospital in North India.

Taneja Vinus V, Khosla Pooja P, Narula Shubhank S, Sachdeva Munish M

The emergence of artemisinin resistance poses a serious global challenge to malaria elimination programs. Artemisinin and its derivatives, especially artesunate, are highly effective against Plasmodium falciparum, particularly in severe and uncomplicated cases. However, increasing reports of treatment failure, particularly with artesunate monotherapy, raise concerns regarding emerging resistance. We present a clinically significant case of suspected artesunate-resistant P. falciparum in an Indian male residing in Nigeria. Despite standard therapy, parasite clearance was delayed, necessitating therapeutic modification. While this case report demonstrates clinical resistance, the lack of confirmatory genetic testing (such as Pfkelch13 mutation screening) remains a limitation.

PMID 42543976
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PubMedZhongguo Zhong yao za zhi = Zhongguo zhongyao zazhi = China journal of Chinese materia medica2026-08-03

[Artesunate enhances effect of leflunomide on inhibiting bone destruction in rheumatoid arthritis via modulating HIF-1α/ARNT signaling pathway].

Huang Feng-Yu FY, Chen Pei-Ping PP, Ding Dai-Yue DY, Wang Qian Q et al.

Based on the hypoxia-inducible factor-1α(HIF-1α)/aryl hydrocarbon receptor nuclear translocator(ARNT) signaling pathway, this study aims to investigate the effects and potential mechanisms of artesunate in enhancing the effect of leflunomide on inhibiting bone destruction in rheumatoid arthritis(RA). By using in vitro osteoclast differentiation model induced by receptor activator of nuclear factor-κB ligand(RANKL) and a collagen-induced arthritis(CIA) mouse model, the intervention effect of combination treatment on bone destruction in RA was systematically evaluated at the cellular, histological, and molecular levels. Key mechanisms were analyzed and screened via transcriptomic sequencing, and relevant mechanisms were further validated through in vitro and in vivo experiments. The results show that artesunate can significantly enhance leflunomide's inhibitory effect on osteoclast formation, further reducing actin ring formation and bone resorption activity. In CIA mice, the combination treatment more effectively decreases the number of tartrate-resistant acid phosphatase(TRAP)-positive multinucleated osteoclasts in the joints compared with leflunomide alone, suggesting that artesunate potentiates leflunomide's ability to inhibit osteoclast formation and differentiation, thereby alleviating bone destruction in RA. Transcriptomic analysis indicates that artesunate may enhance leflunomide's inhibitory effect on bone destruction in RA by modulating the HIF-1α/ARNT signaling pathway. Further validation finds the nuclear co-localization of HIF-1α and ARNT during osteoclast differentiation. The combination treatment markedly suppresses HIF-1α/ARNT signaling and the expression of molecules related to downstream osteoclasts, while upregulating antioxidant-related proteins. The critical role of this signaling pathway in the combination treatment for inhibiting osteoclast differentiation is further supported by using an HIF-1α inhibitor. In summary, this study elucidated the critical role of the HIF-1α/ARNT signaling pathway in artesunate-enhanced leflunomide-mediated amelioration of bone destruction in RA, providing new experimental evidence and theoretical support for understanding the molecular mechanisms of bone destruction in RA and guiding combination treatment with leflunomide.

PMID 42543337
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PubMedTropical biomedicine2026-08-03

The 24-hour crisis: rapidly fatal cerebral malaria due to Plasmodium knowlesi complicated by acute pontine infarction.

Saripudin M H MH, Mokhtar M F MF, Mohd Nor F F

Plasmodium knowlesi is an emerging zoonotic malaria species and a leading cause of malaria in Malaysia. Although severe disease is increasingly recognised, cerebral malaria remains uncommon and is traditionally associated with Plasmodium falciparum. We report a fatal case of cerebral malaria caused by P. knowlesi in a previously healthy 61-year-old woman with a history of frequent orchard visits for peridomestic agricultural activities. She presented with rapid neurological deterioration and circulatory shock, complicated by an acute pontine infarction. Peripheral blood smear and polymerase chain reaction confirmed P. knowlesi infection with a parasite density of approximately 35,000 parasites/ µL. The patient met World Health Organization criteria for severe malaria and was treated promptly with intravenous artesunate in accordance with international guidelines, alongside intensive supportive care for septic shock and multiorgan failure. Despite a rapid reduction in parasitaemia, her condition deteriorated, and she died within 24 hours of presentation. This case highlights the potential for P. knowlesi to cause rapidly progressive and fatal cerebral malaria. Clinicians in endemic regions should maintain a high index of suspicion for zoonotic malaria in patients presenting with acute neurological deterioration.

PMID 42543555
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PubMedFundamental research2026-08-02

Label-free proteomics and single-cell mass cytometry analysis of 5 immune tissues from mice with artesunate administration reveal immunosuppression of artesunate via BST2 and MDSCs.

Hong Rongjian R, Wang Aiting A, Li Yiyang Y, Ding Xianting X

Artesunate is a worldwide prevalent antimalarial medicine, which has also been demonstrated for anti-tumor, anti-virus and anti-autoimmune diseases. Yet the underlying molecular and cellular mechanisms remain largely unexplored. Here, we examined immunological features of 5 immune tissues (spleen, bone marrow, thymus, lymph nodes and peritoneal cavity) of mice with artesunate administration through label-free proteomics and high-dimensional single-cell mass cytometry (CyTOF). Label-free proteomics uncovered dramatic alterations for the interferon-I (IFN-I) induced proteins, especially BST2 and IFIT1 downregulation in spleen and bone marrow. CyTOF analysis further indicated that the percentage of MDSCs was significantly elevated in spleen and bone marrow. The follow-up in vivo LPS-induced inflammatory model confirmed that pretreatment with artesunate attenuated the inflammatory damage, and the expression of BST2 was decreased in the spleen of mice with artesunate administration. Together, our findings presented an immune landscape of multiple tissues of mice with artesunate administration. These datasets provide comprehensive biological resources to develop therapeutic strategies for inflammatory diseases.

PMID 42539575
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PubMedInternational journal of pharmaceutics: X2026-08-02

Artesunate-loaded bovine serum albumin nanoplatform with metal-polyphenol network coating for ferroptosis-driven breast cancer therapy.

Huang Yinghong Y, Zhao Yuanyuan Y, Su Yuhong Y, He Chudong C et al.

Ferroptosis, an iron-dependent programmed cell death process driven by reactive oxygen species (ROS) accumulation, represents a promising therapeutic strategy for breast cancer. However, the efficacy of ferroptosis therapy in breast cancer is often compromised by insufficient intracellular levels of hydrogen peroxide (H2O2) and iron ions. To address these problems, we developed pH-responsive nanoparticles comprising a metal-phenolic network (MPN) shell and a bovine serum albumin (BSA) core for the delivery of artesunate (ART) (designated as BAM NPs). The designed BAM NPs aim to amplify oxidative stress and enhance ferroptosis-based therapy for breast cancer. Upon endocytosis by tumor cells, BAM NPs underwent degradation under acidic conditions to release ART and Fe3+. Subsequently, the reduction of Fe3+ to Fe2+ by glutathione (GSH) initiated the Fenton reaction, which led to aberrant accumulation of ROS. Meanwhile, the endoperoxide bridge of ART could be cleaved by Fe2+ to further generate carbon-centered radicals (·C). Furthermore, BAM NPs effectively deplete GSH via Fe3+/Fe2+ conversion to inactivate glutathione peroxidase 4 (GPX4), thereby disrupting redox homeostasis and increasing intracellular LPO levels. Both in vitro and in vivo experiments showed that BAM NPs significantly inhibited tumor cell proliferation by inducing robust ferroptosis in tumor cells, leading to a tumor inhibition rate of 83.11%. In summary, the constructed BAM NPs served as a promising tailored nanoplatform for augmenting ferroptosis therapy in breast cancer.

PMID 42540475
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