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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

PubMedHorticulture research2026-09-11

AaSnRK2.6 interacts with AaORA to positively regulate artemisinin biosynthesis in Artemisia annua.

Shu Guoping G, Su Fei F, Tang Yueli Y, Li Junnan J et al.

Artemisinin, a sesquiterpene lactone produced in Artemisia annua, is the most effective antimalarial compound, but its low natural abundance in A. annua remains a major bottleneck for large-scale production. Increasing its biosynthesis requires a better understanding of the regulatory networks controlling artemisinin biosynthesis genes. Several jasmonate (JA)-responsive transcription factors have been characterized, but the role of upstream kinases remains poorly understood. Here, we identify AaSnRK2.6, a SnRK2III-type protein kinase, as a novel positive regulator of artemisinin biosynthesis. AaSnRK2.6 expression was strongly induced by methyl jasmonate and abscisic acid, and the protein is localized to both the cytoplasm and nucleus. Protein interaction assays revealed that AaSnRK2.6 specifically interacts with the JA-responsive TF AaORA in the nucleus, and an in vitro kinase assay further showed that AaSnRK2.6 directly phosphorylates AaORA. Dual-luciferase assays showed that AaSnRK2.6 enhances AaORA-mediated activation of key artemisinin biosynthetic genes (amorpha-4,11-diene synthase, DBR2, and ALDH1). Overexpression of AaSnRK2.6 alone or AaORA alone significantly increased artemisinin and dihydroartemisinic acid accumulation, while co-overexpression of AaSnRK2.6 and AaORA in transgenic plants produced the stronger effect. By contrast, RNA interference knockdown of AaSnRK2.6 showed no significant effect on artemisinin levels, likely due to functional redundancy of kinases. Collectively, this study supports a positive kinase-TF regulatory module involved in hormone-responsive artemisinin biosynthesis in A. annua and provides new insights into its regulatory mechanism.

PMID 42723713
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PubMedGates open research2026-09-11

Structural and Functional Impact of the G340S Mutation in Plasmodium falciparum Ferredoxin NADP⁺ Reductase: In silico Analysis and Molecular Docking.

Kiboi Daniel D, Muriithi Brenda B

Plasmodium falciparum, the deadliest malaria parasite, continues to burden health systems across sub-Saharan Africa, where artemether-lumefantrine remains a frontline treatment. Partial artemisinin resistance is emerging, increasing selection pressure on lumefantrine (LM), yet the molecular basis of reduced LM susceptibility remains poorly defined. While LM has been described as refractory to resistance, its efficacy could be compromised if resistance arises. To explore candidate determinants of LM response and guided by a Gly332Ser substitution previously identified in Ferredoxin NADP + reductase from LM-selected Plasmodium berghei, we investigated the homologous G340S variant in Plasmodium falciparum ferredoxin NADP + reductase ( PfFNR), a central enzyme of the apicoplast redox system. To predict the structural and functional impact of the G340S substitution, this study integrated sequence conservation analysis, AlphaFold 3 structural modelling, structural superimposition, molecular dynamics simulation, NADPH and NADP + docking, HADDOCK docking with P. falciparum ferredoxin ( PfFd), and comparative docking of lumefantrine, primaquine, artemisinin and dihydroartemisinin. Gly340 was conserved across the Plasmodium FNR orthologs examined and mapped to a constrained loop adjacent to the NADP + binding region. Structural superimposition showed that G340S preserved the global PfFNR fold but introduced localized changes near residue 340. Exploratory single-trajectory molecular dynamics suggests that G340S may alter PfFNR conformational sampling, with increased RMSD, radius of gyration, solvent-accessible surface area and residue-level flexibility. Cofactor docking predicted a modest mutation-associated shift, strongest for NADPH, whereas NADP + docking remained largely stable. HADDOCK analysis indicated altered PfFNR-PfFd docking preferences, and antimalarial docking showed ligand-dependent effects, greatest for artemisinin and dihydroartemisinin, with minimal lumefantrine change. Together, these data support G340S as a redox-associated candidate variant that may reshape cofactor and partner-interface, but not as a validated lumefantrine-resistance marker until confirmed by biochemical, genetic and parasite-based assays. The findings define testable mechanisms for future functional assays of PfFNR in antimalarial response phenotypes.

PMID 42723717
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PubMedJournal of clinical pharmacology2026-09-10

Pharmacokinetics and Pharmacodynamics of Antimalarial Agents: Optimizing Combination Therapies to Overcome Resistance Mechanisms.

Pica Kiana K, Grundmann Oliver O, Azeredo Francine Johansson FJ

Malaria remains a persistent global health challenge, worsened by the emergence of drug-resistant Plasmodium strains. This review synthesizes the pharmacokinetics (PK) and pharmacodynamics (PD) of key antimalarial agents, evaluating how these properties influence the performance of current pharmacological regimens. Findings in the literature indicate that artemisinin-based combination therapies (ACTs) achieve rapid parasite clearance by using short-acting artemisinin derivatives paired with longer-acting partner drugs. PK/PD modeling consistently demonstrates that well-matched half-lives and sustained post-treatment exposure are critical to prevent functional monotherapy-related resistance. Non-artemisinin and triple combination regimens show promise in overcoming multidrug resistance, but gaps remain in exposure-response characterization, dose alignment, and population-specific optimization. A discussion of PK/PD modeling across agents, including chloroquine, artemisinin and its derivatives, mefloquine, primaquine, and tafenoquine, highlights how inadequate drug exposure, mismatched partner drug kinetics, and host metabolic variability contribute to treatment failure. Collectively, the evidence suggests that refining combination regimens through PK/PD-guided dose optimization is crucial for maintaining efficacy and preventing resistance. Future research must prioritize host-specific factors, stage-specific drug activity, and optimized combination regimens to improve therapeutic outcomes and support malaria eradication.

PMID 42717725
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PubMedPhytomedicine : international journal of phytotherapy and phytopharmacology2026-09-10

Artesunate potentiates poly (ADP-ribose) polymerase inhibitor efficacy in ovarian cancer through RAD51-mediated homologous recombination repair impairment.

Zhou Shimin S, Xue Lujiadai L, Li Guiqing G, Huang Lilin L et al.

The homologous recombination repair (HRR) RAD51 recombinase is essential for ensuring accurate DNA repair, and its expression levels are inversely correlated with Poly (ADP-ribose) Polymerase inhibitor (PARPi) sensitivity. Artesunate (ART), a semisynthetic water-soluble sesquiterpene lactone derived from artemisinin, a natural product of Artemisia annua, was previously identified from an HRR reporting system as a potential HRR modulator, suggesting its utility as a PARPi sensitizer. The clinical relevance of RAD51 was assessed using the TCGA database. In vitro studies employed A2780 and SKOV3 ovarian cancer cell lines, utilizing RAD51 siRNA, the inhibitor IBR2, and ART alone or in combination with Olaparib (Ola). Used cell counting kit-8, colony formation, and EdU assays to evaluate cell proliferation.; apoptosis by flow cytometry; and DNA damage by γ-H2AX immunofluorescence and comet assays. Protein levels were analyzed by Western blotting (p-ATM, γ-H2AX, RAD51). The ART-RAD51 interaction was validated via cellular thermal shift assay, drug affinity responsive target stability, and molecular docking. In vivo efficacy and safety were evaluated in a nude mouse xenograft model. RAD51 expression was correlated with ovarian cancer progression, and PARPi treatment itself promoted RAD51 expression. siRNA and inhibitior of RAD51 sensitized ovarian cells to Ola. We identified ART as a direct inhibitor of RAD51, which binds to RAD51 and promotes its protein degradation, thereby inhibiting HRR. The combination of ART and Ola significantly increased DNA damage, inhibited proliferation, and induced apoptosis in vitro. This combination also potently suppressed tumor growth in vivo without observable significant toxicity. Our findings establish RAD51 as a key target for addressing PARPi-resistant in ovarian cancer. We demonstrate that ART counteracts this resistance through directly binding to and degrading RAD51, thereby inhibiting HRR. The ART-Ola combination presents a novel, synergistic, and well-tolerated strategy in preclinical models, providing a strong mechanistic rationale for future clinical translation.

PMID 42721822
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PubMedAntimicrobial agents and chemotherapy2026-09-09

Functional validation of the Plasmodium falciparum K13 C580Y mutation in recently collected Ethiopian isolates.

Mukherjee Angana A, Assefa Ashenafi Bahita AB, Turlo Christopher V CV, Needham Lisa Checkley LC et al.

Recent genomic investigation in Ethiopia identified the first detection of the Plasmodium falciparum Kelch13 (K13) C580Y substitution in the Horn of Africa. To assess its functional impact, we introduced C580Y into two recently collected Ethiopian clinical isolates using CRISPR-Cas9 genome editing. Ring-stage survival assays showed significantly elevated in vitro dihydroartemisinin survival in edited parasites relative to isogenic controls, demonstrating that C580Y confers artemisinin tolerance in contemporary Ethiopian parasite genetic backgrounds.

PMID 42714387
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PubMedJournal of gastrointestinal oncology2026-09-08

Artemisinin inhibits colorectal cancer progression via the FAM83A-AS1/HIF-1α axis.

Xi Jinchuan J, Li Zhihan Z, Liu Youqiang Y, Li Zheng Z et al.

Emerging evidence indicates that the lncRNA FAM83A-AS1 interacts closely with HIF-1α to modulate malignant biological behaviors and glycolytic metabolism in CRC. The mechanism underlying the effects of artemisinin on colorectal cancer (CRC) was investigated using a network pharmacology approach. The action network of artemisinin was analyzed using network pharmacology. Stable FAM83A-AS1 and HIF-1α knockout cell models were established using a lentiviral system. The effects of artemisinin on cellular functions, including proliferation, metastasis, cell cycle progression, and glycolysis in CRC cells, were assessed through in vitro assays. The expression of HIF-1α was assessed by immunohistochemistry in tumor tissues from 219 patients with CRC, and its clinical associations were analyzed. Artemisinin was predicted to target 96 proteins associated with CRC, including HIF-1α. Artemisinin inhibited proliferation, migration, and glycolysis, and induced cell cycle arrest in CRC cells. Artemisinin reduced the expression levels of Cyclin D1, CDK4, HIF-1α, PKM2, and N-cadherin. Artemisinin promoted proteasome-mediated degradation of HIF-1α protein. HIF-1α upregulated the expression of FAM83A-AS1, whereas knockdown of FAM83A-AS1 reduced HIF-1α expression levels. The expression level of HIF-1α in tumor tissues was significantly higher than that in adjacent non-tumor tissues. HIF-1α expression was associated with tumor node metastasis (TNM) stage, tumor (T)​stage, node (N)​stage, carcinoembryonic antigen (CEA) levels, recurrence, metastasis, and prognosis in patients with CRC. Artemisinin promoted proteasome-mediated degradation of HIF-1α protein and inhibited CRC progression, potentially through the FAM83A-AS1/HIF-1α regulatory axis.

PMID 42707883
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