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artemisinin + amodiaquin (ASAQ / Winthrop / Coarsucam)

✓ Approved

DNDi · Small Molecule · Small Molecule

What is artemisinin + amodiaquin?

artemisinin + amodiaquin is a small molecule developed by DNDi. It is approved for therapeutic indications via oral (po).

Drug Profile

Brand NamesASAQ, Winthrop, Coarsucam
CompanyDNDi
Drug ClassSmall Molecule
RouteOral (PO)
StatusApproved
Sources: ClinicalTrials.gov, DNDi

Therapeutic Indications

artemisinin + amodiaquin is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Infections and infestationsPlasmodium malariae infection✓ Approved

Related Research Articles

PubMedCritical reviews in eukaryotic gene expression2026-10-13

Dihydroartemisinin Suppresses Esophageal Squamous Cell Carcinoma by Downregulating COX-2 through the ROS/MAPK/Sp1 Pathway.

Liao Chongbo C, Zhu Xingyao X, Yang Yong Y, Zhu Jiang J et al.

Esophageal squamous cell carcinoma (ESCC) has a poor prognosis due to its aggressiveness and chemoresistance, necessitating novel therapeutic strategies. Dihydroartemisinin (DHA), an artemisinin derivative, exhibits broad anticancer activity, but its mechanism in ESCC remains incompletely understood. Transcriptomic sequencing identified differentially expressed genes upon DHA treatment. The regulation of COX-2 by DHA was validated via RT-qPCR and Western blot. Gain- and loss-of-function assays assessed COX-2 and Sp1 effects on ESCC proliferation and migration. Dual-luciferase reporter assays confirmed Sp1-driven COX-2 transcription. ROS levels and MAPK pathway protein expression were measured by flow cytometry and Western blot, respectively. A xenograft model evaluated in vivo effects of Sp1 overexpression and DHA. DHA downregulated COX-2 in a time- and dose-dependent manner, inhibiting ESCC cell proliferation and migration. Sp1 directly bound the COX-2 promoter and positively regulated its expression, thereby promoting malignant phenotypes. DHA triggered ROS accumulation and downregulated the protein levels of MAPK (ERK/MSK), Sp1, and COX-2. Both NAC (an antioxidant) and Sp1 overexpression reversed these effects. In vivo, DHA significantly suppressed tumor growth via the Sp1/COX-2 axis without detectable toxicity. This study establishes that DHA inhibits ESCC proliferation and metastasis through the ROS-MAPK(ERK/MSK)-Sp1-COX-2 axis, highlighting DHA as a promising repurposed agent and identifying Sp1/COX-2 as novel therapeutic targets for ESCC.

PMID 42868586
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PubMedPhytomedicine : international journal of phytotherapy and phytopharmacology2026-10-13

Artemisitene targets GLIS3 to inhibit the NF-κB-TNF signaling pathway and suppress bladder cancer cell growth.

Li Kai K, You Ganhua G, Liu ZiJing Z, Cheng Xiaotao X et al.

Artemisia annua, a medicinal and edible herb best known for Artemisinin, exhibits broad pharmacological activities and considerable clinical value. However, its therapeutic potential in bladder cancer remains largely unexplored. Here, we systematically investigated the anti-bladder cancer efficacy of Artemisitene (ATT) in vitro and in vivo and delineated its underlying mechanisms. Using cell-based and animal models, we found that ATT robustly suppressed bladder cancer cell growth. Integrated transcriptomic and proteomic sequencing, combined with MST assays and transient transfection, revealed the mechanism of ATT inhibiting the progression of bladder cancer. In addition, we analysed single-cell RNA-sequencing datasets and performed virtual knockout experiments to investigate the expression pattern and potential functional role of the ATT target gene GLIS3 across different pathological stages of bladder cancer. GLIS3 expression was higher in tumour than in adjacent nontumor tissues in BLCA patients and was further elevated in intermediate/late stages (T3-T4) compared with early stages (T1-T2). Consistently, single-cell RNA-seq data showed that GLIS3 levels in epithelial cells were higher in T3-T4 than in T1-T2 BLCA. Moreover, in virtual GLIS3 knockout in BLCA epithelial cells negatively regulated TNF and NF-κB signalling pathways. ATT directly interacts with GLIS3 and destabilizes the protein, consequently suppressing the transcription of NF-κB and TNF. Mutation of GLIS3 at Arg-404 and Pro-411 markedly weakened its interaction with ATT and partly abrogated the pharmacological effects of ATT. Moreover, GLIS3 knockdown enhanced the inhibitory effect of Gem on bladder cancer cells, while ATT further potentiated Gem-mediated suppression of BLCA by downregulating GLIS3 expression. ATT binds to GLIS3 and decreases its protein stability, thereby suppressing the transcription of NF-κB and TNF, inducing apoptosis in bladder cancer cells, and inhibiting cell proliferation, migration, and invasion. These findings provide a mechanistic rationale for developing ATT as a potential therapeutic agent or dietary supplement for bladder cancer and expand the medicinal value of Artemisia annua derivatives.

PMID 42863415
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PubMedActa tropica2026-10-13

Dendrimer-Based Nano Artesunate/β-Glucan as a Promising Antimalarial Candidate: Insights from in Vivo Evaluations.

Noorzaei Mahla M, Khanabadi Faride F, Alimardan Zahra Z, Akbariqomi Mostafa M et al.

Malaria remains a major global health burden, with increasing concerns regarding resistance to conventional antimalarial therapies, including artemisinin derivatives. This study aimed to develop and evaluate a second-generation dendrimer-based nano artesunate/β-glucan formulation designed to combine antiplasmodial activity with potential immunomodulatory effects against malaria. A nano artesunate/β-glucan nanocomposite was synthesized using a G2 dendrimer platform and characterized by dynamic light scattering (DLS), scanning electron microscopy (SEM), Fourier-transform infrared spectroscopy (FTIR), drug loading analysis, solubility assessment, and release kinetics. Antimalarial efficacy was evaluated in a murine Plasmodium berghei model using parasitemia monitoring, lactate dehydrogenase (LDH) assays, and survival analysis. Immunomodulatory effects were assessed through macrophage nitric oxide (NO) production and serum interferon-gamma (IFN-γ) levels. Toxicological evaluation included body weight monitoring, erythrocyte morphology and hemolysis assays, liver enzyme analysis, and histopathological examination of hepatic tissues. The synthesized nanocomposite showed a mean particle size of 157.5 nm, acceptable size distribution (PDI = 0.284), and spherical morphology. Loading into the dendrimer-based nanocomposite improved the aqueous solubility of artesunate and β-glucan by 83% and 27%, respectively, and enabled sustained drug release over 48 hours. In vivo, the nano artesunate/β-glucan formulation at 100 mg/kg and 80 mg/kg, respectively, achieved complete parasite clearance within 4 days, with no recrudescence during the 21 days of follow-up. This effect was accompanied by increased NO and IFN-gamma levels, suggesting possible immune involvement. Compared with free artesunate and chloroquine, the nanocomposite showed lower hepatotoxicity, minimal hemolysis, preserved erythrocyte morphology, and only minor liver histopathological changes. The dendrimer-based nano artesunate/β-glucan formulation showed potent antiplasmodial activity, improved solubility, sustained release, and a favorable acute safety profile in a murine malaria model. It may represent a promising antimalarial nano formulation, although further mechanistic and long-term safety studies are needed.

PMID 42869154
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PubMedFrontiers in cellular and infection microbiology2026-10-11

Assessing the threat of artemisinin resistance: seasonal and ecological patterns of PfKelch13 mutation distribution in malaria-endemic communities in Ghana.

Dakorah Mavis Puopelle MP, Aninagyei Enoch E, Adzakpah Godwin G, Attoh Juliana J et al.

Resistance to Artemisinin-based combination therapies (ACTs) threatens the backbone of Ghana's success in Malaria control. In addition, malaria remains prevalent in the Central Region, raising concerns about the potential emergence of drug resistance. Mutations in the PfKelch13 gene associated with reduced susceptibility have been reported across Africa and in some parts of Ghana, highlighting the need for molecular surveillance in these endemic settings. Dried blood spots were prepared from whole blood, and genomic DNA was amplified using established Plasmodium-specific primers. Selective whole-genome amplification enriched Plasmodium falciparum DNA, and libraries were sequenced using high-throughput Illumina HiSeq 2500 technology. 358 samples were successfully sequenced. PfKelch13 wild-type (WT) allele remained predominant, ranging from 42% to 100%, but the burden and diversity of mutant alleles differed substantially by location. SNPs observed were 127 single mutations, 42 double mutations, 2 Triple mutations, and 1 Quadruple mutation. Neither the ecological zone nor the season was significantly associated with the occurrence of mutant haplotypes; however, the district of origin emerged as statistically significant. The study demonstrates the presence of PfKelch13 mutations in Plasmodium falciparum in the Central Region of Ghana, with substantial genetic diversity but low frequencies of validated resistance markers. The spatial and seasonal heterogeneity observed across transmission settings suggests that factors operating at finer geographical and temporal scales may be important determinants of genetic variation, highlighting limitations of broad ecological classifications. These findings underscore the need for continuous, fine-scale molecular surveillance and therapeutic efficacy studies to detect and mitigate emerging artemisinin resistance proactively.

PMID 42856927
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PubMedBioMed research international2026-10-10

Genomic Plasticity and Molecular Mechanisms of Antimalarial Drug Resistance in Plasmodium falciparum: Implications for Treatment Failure and Genomic Surveillance.

Assemie Anmut A

Malaria remains a major global public health challenge, in part because Plasmodium falciparum populations can acquire and disseminate reduced susceptibility to antimalarial drugs under selective pressure. This review synthesizes current evidence on the molecular and genomic mechanisms underlying antimalarial drug resistance and examines their implications for treatment efficacy and malaria control. First, the review examines genomic plasticity, including structural genome variation, copy-number variation, recombination, epigenetic regulation, and transcriptional regulation, as sources of genetic and phenotypic variation relevant to drug susceptibility. Second, it summarizes established molecular determinants of resistance, including kelch13 (K13) mutations associated with delayed parasite clearance following artemisinin treatment, pfcrt mutations associated with chloroquine resistance, pfmdr1 copy-number variation associated with altered susceptibility to mefloquine and related antimalarials, and dhfr and dhps mutations associated with sulfadoxine-pyrimethamine resistance. Third, the review considers the emergence and dissemination of resistance-associated variants across parasite populations, emphasizing the contributions of population genomics and genomic surveillance to monitoring resistance patterns. Finally, recent applications of genomic epidemiology, whole-genome sequencing, and artificial intelligence-assisted analytical approaches are discussed, with emphasis on their potential utility for resistance surveillance and evidence-informed malaria control. Overall, integrating molecular, genomic, epidemiological, and evolutionary information provides a stronger framework for understanding antimalarial resistance and for supporting surveillance, treatment optimization, and malaria-control strategies.

PMID 42855825
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PubMedACS omega2026-10-09

Endoperoxides Show Distinct Reactivity toward Heme and Hemoglobin.

Wang Shuang S, Sun Jiubo J, Wei Chunyan C, Zhang Chong-Jing CJ

Artemisinin and Yingzhaosu A (YZSA), two endoperoxide-containing natural products with antimalarial activity discovered through China's historic 523 Project, have long been the focus of global antimalarial research. Many scientific studies have proposed that their endoperoxide bridges are activated by heme (not hemoglobin) to generate active carbon radicals, which subsequently eliminate the parasite. However, we discovered that X-2b, a YZSA-structured turn-on fluorescent probe previously reported by our group, exhibited stronger reactivity toward hemoglobin than toward heme, a finding that prompted us to revisit and refine our previously reported conclusions. Herein, we present a systematic investigation into the reactivity of several representative endoperoxide-containing compounds toward heme and hemoglobin. The investigated endoperoxides show distinct reactivity toward heme versus hemoglobin. Notably, compounds showing high reactivity toward hemoglobin display diminished antimalarial activity. This study challenges the prevailing mechanistic paradigm and sheds new light on the mode of action of endoperoxide-containing antimalarials.

PMID 42851826
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