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artemisinin + amodiaquin (ASAQ / Winthrop / Coarsucam)

✓ Approved

DNDi · 小分子 · 小分子

什么是 artemisinin + amodiaquin？

artemisinin + amodiaquin 是一种小分子，由DNDi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ASAQ, Winthrop, Coarsucam
公司DNDi
药物类别小分子
给药途径Oral (PO)
状态Approved
来源： ClinicalTrials.gov, DNDi

治疗适应症

artemisinin + amodiaquin 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
Infections and infestationsPlasmodium malariae infection✓ Approved

相关研究文献

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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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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PubMedPakistan journal of pharmaceutical sciences2026-09-08

Artemisinin alleviates hippocampal neuronal apoptosis and cognitive impairment in rats after cardiac arrest resuscitation: Association with the PI3K/Akt pathway.

Gao Yuanyuan Y, Han Shuwen S, Lu Yaojun Y, Zhao Junli J

Cardiac arrest (CA) is associated with high mortality and severe neurological sequelae. Artemisinin (ARS), a natural product from Artemisia annua, has potential neuroprotective effects, but its role in brain injury after CA resuscitation remains unclear. This study investigated the effects of ARS on hippocampal neuronal apoptosis and cognitive dysfunction in rats after CA resuscitation and explored whether these effects are associated with the phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) signaling pathway. Sixty male rats were randomly assigned to six groups: sham, model, artemisinin (40 mg/kg), dimethyl sulfoxide ((DMSO, 100 mg/kg), LY294002 (a phosphatidylinositol 3-kinase inhibitor, 25 mg/kg) and artemisinin plus LY294002. Cardiac arrest was induced by transcutaneous electrical stimulation. Outcome assessors were blinded. Neurological function was evaluated using the Neurological Deficit Scale. Hippocampal damage and apoptosis were assessed by hematoxylin and eosin staining and terminal deoxynucleotidyl transferase dUTP nick end labeling staining. Learning and memory were tested using novel object recognition and the Morris water maze. Protein expression was measured by Western blot. Artemisinin significantly improved Neurological Deficit Scale scores, reduced terminal deoxynucleotidyl transferase dUTP nick end labeling-positive cells and alleviated hippocampal damage. Artemisinin also prolonged novel object exploration time, shortened escape latency, increased target quadrant time and upregulated phosphatidylinositol 3-kinase expression and the ratio of phosphorylated protein kinase B to protein kinase B. Co-administration of LY294002 partially reversed these effects. Artemisinin alleviates hippocampal neuronal apoptosis and improves neurological deficits and cognitive dysfunction in rats after cardiac arrest resuscitation, suggesting a possible association with activation of the phosphatidylinositol 3-kinase/protein kinase B pathway. Limitations include use of a single pharmacological inhibitor and lack of genetic validation.

PMID 42708788
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PubMedAnalytical chemistry2026-09-08

Small-Molecule Interaction-Driven Luminol-Artemisinin Chemiluminescent Probe for Highly Sensitive Determination of Alkaline Phosphatase.

Suleiman Mohammed Y MY, Ma Jintao J, Hosseinkhani Saman S, Nikkhah Maryam M et al.

Alkaline phosphatase (ALP) is a pivotal enzyme in diverse physiological processes, and its activity serves as an essential biomarker in clinical diagnostics and biomedical research. The development of reliable and highly sensitive assays for monitoring ALP is therefore of great importance. Herein, we present a luminol-artemisinin (ART) chemiluminescence (CL) platform for the ultrasensitive determination of ALP activity. The assay relies on ALP-catalyzed hydrolysis of ascorbic acid 2-phosphate (AA2P) to produce ascorbic acid (AA), which efficiently quenches luminol-ART CL. Systematic optimization, sensitivity, and selectivity studies revealed a strong correlation between ALP concentration and the quenching of the CL intensity, enabling quantitative analysis with high sensitivity and excellent selectivity. The assay was further validated using human serum samples from healthy donors and patients with clinically documented elevated ALP levels. In healthy diluted serum samples, the standard addition method yielded endogenous ALP activities of 0.104-0.118 U L-1 with recoveries of 97.01-107.89%. Furthermore, the ALP activities in diluted serum samples from three clinical patients were determined to be 0.347, 0.183, and 0.221 U L-1, in close agreement with the corresponding clinical reference values of 0.353, 0.171, and 0.226 U L-1, demonstrating the accuracy and practical applicability of the proposed assay. Compared with existing analytical techniques, the luminol-ART CL assay provides superior sensitivity, operational simplicity, and compatibility with complex biological matrices, offering a promising platform for clinical diagnostics and biochemical analysis.

PMID 42708743
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PubMedPLoS pathogens2026-09-08

Dual plasmepsin IX and X inhibitors are refractory to development of resistance.

Favuzza Paola P, Dans Madeline G MG, Su Wenyin W, Thompson Jennifer K JK et al.

Artemisinin-based combination therapies (ACTs) remain the cornerstone of malaria treatment, but emerging resistance threatens their efficacy. The potential for the development of drug resistance against plasmepsin X (PMX)-selective inhibitors and dual plasmepsin IX/X (PMIX/X) inhibitors was investigated in Plasmodium falciparum. A series of PMX-selective (WM4, WM76, WM92) and PMIX/X dual inhibitors (WM382, WM09, WM42) were characterised for potency against parasite growth and enzyme inhibition. In vitro selection experiments showed that all compounds had a high barrier to resistance, although parasites with reduced sensitivity to PMX‑selective inhibitors could still be selected. Resistance mechanisms involved pmx gene amplification and point mutations (D245N, S315P, S359P, I363L) that alter inhibitor binding. Recombinant expression and Michaelis-Menten kinetics demonstrated that these mutations impair drug binding whilst preserving PMX catalytic function. Reverse genetics confirmed that introducing these mutations into the pmx gene resulted in decreased potency of the inhibitors. In this study, resistance to the PMIX/X dual inhibitors evaluated here could not be selected, despite prolonged selection pressure. Antimalarial Resistome Barcoding (AReBar) assays confirmed the absence of pre-existing resistance to either inhibitor class. Critically, PMIX/X dual inhibitors maintained efficacy against parasites with decreased sensitivity to PMX-selective compounds. These findings demonstrate that dual PMIX/X inhibitors present a substantially higher barrier to resistance than PMX-selective inhibitors, informing antimalarial drug development strategies and highlighting dual-target inhibition as a promising approach to mitigate resistance risks.

PMID 42709875
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