Drug Database
AR

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

PubMedActa tropica2026-05-24

Status of pfcrt and pfmdr1 mutations in Plasmodium falciparum isolates in Gabon in 2019 after chloroquine withdrawal.

Dinzouna-Boutamba Sylvatrie-Danne SD, Iroungou Berthe Amélie BA, Akombi Falone Larissa FL, Yacka-Mouele Lauriane L et al.

Chloroquine (CQ) resistance has long contributed to antimalarial treatment failure. Despite the implementation of artemisinin-based combination therapies (ACTs) in Gabon, continued surveillance of antimalarial drug resistance markers remains essential for malaria control and elimination. This study aimed to monitor molecular markers of antimalarial drug resistance, specifically the Plasmodium falciparum chloroquine resistance transporter (pfcrt) and P. falciparum multidrug resistance 1 (pfmdr1), in P. falciparum clinical isolates from Libreville, nearly two decades after CQ withdrawal. Archived dried blood spots collected in 2019 were retrieved to assess the prevalence of pfcrt and pfmdr1 mutations and haplotypes in P. falciparum isolates. In total, 70 samples were successfully genotyped via Sanger sequencing. Single nucleotide polymorphisms (SNPs) associated with antimalaria drug resistance were identified in 25.71% of pfcrt and 20% of pfmdr1. For pfcrt, the most frequent mutation was N75(E/K) (24.3%), followed by M74I (22.86%) and K76T (17.14%). Moreover, malaria-positive individuals exhibited mainly the wild-type haplotype CVMNK (74.29%), while the mutant haplotype CVIET (17.13%) was the most common among the mutant variants. The frequency of CVIET observed in this study is substantially lower than the previously reported frequency in Gabon. Other mutant haplotypes, including CVINK, CVMEK, CVMNT, CVIEK, and CVIKK, were each detected at low frequencies (1.43%). Similarly, for pfmdr1, the most frequent mutation was Y184F (18.57%), which predominantly produced the mutant haplotype NEFND (15.71%), compared with YEFND (2.86%) and NEYDD (1.43%). Nevertheless, the wild-type haplotype NEYND was observed in 80% of the study population. These finding indicate the persistence of mutant genotypes in both pfcrt and pfmdr1, along with a decline in their frequencies over time, suggesting a progressive restoration of CQ susceptibility. The results underscore the importance of longitudinal CQ resistance monitoring to accurately assess its prevalence and inform public health interventions.

PMID 42176722
Read full article →
PubMedThe Journal of antimicrobial chemotherapy2026-05-22

Updated mapping of Plasmodium falciparum kelch13 gene polymorphisms in Madagascar, 2024.

Roesch Camille C, Ratovoson Rila R, Delaunay Constance C, Savary Sharon S et al.

Artemisinin-resistant Plasmodium falciparum has emerged in several East African countries neighbouring Madagascar. Despite the island's substantial malaria burden, recent data on artemisinin partial resistance are limited, raising concerns about the potential emergence of resistant parasites. This study provides an updated overview of the prevalence and diversity of P. falciparum Kelch13 (pfkelch13) polymorphisms in Madagascar. During a nationally representative, cross-sectional survey conducted between January and May 2024, dried blood samples were collected from 4850 febrile patients at 65 health facilities. Pfkelch13 genotyping was performed using a targeted amplicon deep sequencing approach. Of the 1944 P. falciparum-positive samples, 963 (49.5%) pfkelch13 sequences were successfully obtained, and 885 (91.9%) corresponded to the 3D7 wild-type. Non-synonymous and synonymous mutations were detected in 1.8% (17/963) and 6.2% (60/963) of isolates, respectively, whereas one isolate (0.1%) carried double mutations. Of the 18 mutations identified, 5 had not been previously reported. The two most frequent polymorphisms in Madagascar were the synonymous mutations C469C (3.0%, 29/963) and P417P (2.8%, 27/963). None of the WHO-validated artemisinin partial resistance markers were detected. This study provides an updated baseline of pfkelch13 polymorphisms in Madagascar, with no evidence of artemisinin partial resistance emergence. Importantly, no parasites harbouring a validated artemisinin resistance marker were detected across the regions sampled, suggesting that resistant parasites have not yet become established. These findings provide a valuable baseline for future genomic surveillance efforts aimed at the early detection of mutations associated with artemisinin partial resistance.

PMID 42169509
Read full article →
PubMedPathology, research and practice2026-05-22

Dihydroartemisinin alleviates dextran sulfate sodium-induced colitis in mice: Associations with gut microbiota, arachidonic acid metabolism, and the IL-17 signaling pathway.

Chen Wei W, Xu Lin L, Wang Meng M, Li Yan Y et al.

Dihydroartemisinin (DHA), a sesquiterpene lactone derived from artemisinin, exhibits well-documented anti-inflammatory and anti-cancer properties. However, the precise mechanisms through which DHA alleviates ulcerative colitis (UC) remain incompletely understood. This study aimed to investigate the effects and underlying mechanisms of DHA on dextran sulfate sodium (DSS)-induced colitis in mice using a multi-omics approach, including 16S rRNA microbiomics, non-targeted and targeted metabolomics, RNA-seq transcriptomics and network pharmacology analysis. A DSS-induced murine colitis model was established and treated with DHA. Disease activity, colonic pathology, and intestinal barrier function were assessed. Gut microbiota composition was analyzed via 16S rRNA sequencing, while colonic metabolites were profiled using non-targeted metabolomics. Key signaling pathways associated with DHA treatment were predicted through RNA-seq and network pharmacology, and further validated by qRT-PCR and flow cytometry. Antibiotic depletion experiments were performed to evaluate the role of the gut microbiota. Intestinal barrier integrity was examined by immunofluorescence, western blot, and AB/PAS staining. Targeted metabolomic analysis of specific colonic metabolites was conducted using the Q300 kit. DHA treatment significantly ameliorated colitis symptoms, as indicated by reduced body weight loss, lower disease activity index (DAI) scores, attenuated colon shortening, and improved histopathology. DHA treatment correlated with restored intestinal barrier function including increased goblet cell numbers, enhanced mucin-2 expression, and upregulating tight junction proteins. It was also associated with mitigated gut microbiota dysbiosis, notably including restored abundance of Bifidobacterium and suppressed opportunistic pathogens. Non-targeted metabolomics revealed that DHA treatment was associated with significant changes in arachidonic acid metabolism. Integrated transcriptomics and network pharmacology analysis indicated that DHA treatment was correlated with suppression of the IL-17 signaling pathway and restoration of Th17/Treg balance in colonic tissues. Crucially, the therapeutic benefits of DHA were abolished in microbiota-depleted mice, manifested as loss of mucosal protection, absence of IL-17 pathway and Th17/Treg balance modulation, and no significant alteration in arachidonic acid levels as detected by targeted metabolomics. Our findings highlight the multifaceted therapeutic potential of DHA in colitis treatment, and suggest that the gut microbiota is associated with its protective effects. The beneficial effects observed with DHA treatment are correlated with preservation of intestinal barrier integrity, restoration of microbial homeostasis, changes in arachidonic acid metabolism, and modulation of the IL-17 pathway and Th17/Treg balance. These insights provide promising directions for novel UC therapeutic strategies.

PMID 42166934
Read full article →
PubMedMalaria journal2026-05-21

Plasmodium falciparum antimalarial resistance in Angola: a systematic review.

Matias Daniela D, Chaves Celso C, Cândido Ana Micolo AM, Morais Joana J et al.

Malaria remains a major health challenge in Angola, where Plasmodium falciparum accounts for most cases and deaths. Although artemisinin-based combination therapies (ACTs) have been the recommended first-line treatments in the country since 2006, the emergence of resistance-associated mutations in Africa raises concerns. We conducted a systematic review of molecular markers of antimalarial drug resistance in Angola (2000-2024) to map their prevalence and distribution at the provincial level. Following PRISMA 2020 guidelines, we searched PubMed, Scopus and Web of Science for studies on P. falciparum resistance markers: polymorphisms in pfcrt, pfdhfr, pfdhps, pfmdr1, pfk13, or copy number variation (CNV) in pfmdr1 and pfpm2/3. Data on mutations, prevalence, and geographic distribution was extracted and summarized. 20 studies met our inclusion criteria. The chloroquine-resistant pfcrt CVIET haplotype persisted in northern and coastal provinces, while the SP-resistant pfdhfr/pfdhps IRNGE haplotype was detected in Cabinda and Zaire. No validated pfk13 mutations linked to artemisinin resistance were reported. Pfmdr1 analyses showed declining 86Y and 1246Y mutation frequencies, with wild-type NYD and NFD haplotypes predominating. Low pfmdr1 and pfpm2 CNV prevalence was reported, though recent data indicate emerging amplification in southern Angola. Research was concentrated in Benguela, Luanda, Lunda Sul, and Zaire, leaving large geographic gaps country-wise. Resistance markers in Angola show heterogeneous provincial distribution. Expanded molecular surveillance, particularly in underrepresented provinces and among pregnant women, is critical to safeguard ACT efficacy and guide national malaria control strategies.

PMID 42163265
Read full article →
PubMedExperimental animals2026-05-21

Artesunate ameliorates experimental colitis by suppressing intestinal inflammation and modulating the gut microbiota.

Sun Haiyang H, Jiang Rujiao R, Jing Jingjing J, Wang Xinying X et al.

Artesunate (ART) is a semi-synthetic derivative of artemisinin with well-established antimalarial activity. In this study, we demonstrate that ART treatment markedly attenuates disease severity in dextran sulfate sodium (DSS)-induced colitis. ART significantly reduces the accumulation of inflammatory neutrophils, monocytes, Th17 cells, and IL-17-producing ILCs and γδT cells in the colon, accompanied by suppression of pro-inflammatory gene expression, including Tnf, Il6, and Il1b, and upregulation of anti-inflammatory mediators such as Tgfb and Il10. In parallel, ART restores the expression of intestinal tight junction proteins ZO-1 and claudin-1, indicating improved epithelial barrier integrity. ART treatment inhibits the IL-17 production from both Th17 cells and other lymphocytes. ART also reshapes the gut microbiota, which contributes to protection against DSS-induced colitis. Notably, mesalazine co-treatment with ART augmented its protective efficacy against DSS-induced colitis. Collectively, these findings identify ART as a potent modulator of intestinal inflammation and barrier function, highlighting its therapeutic potential for mucosal inflammatory diseases.

PMID 42161523
Read full article →
PubMedThe Lancet. Microbe2026-05-20

Artemether-lumefantrine for the treatment of Plasmodium falciparum malaria in Laos: a therapeutic efficacy study coupled with genomic and in vitro phenotypic analyses.

Feufack-Donfack Lionel B LB, Khim Nimol N, Tat Baura B, Banouvong Virasack V et al.

Artemisinin-based combination therapies (ACTs) have played a crucial role in decreasing the impact of malaria worldwide. Since 2005, artemether-lumefantrine (AL) has been the main first-line treatment for uncomplicated Plasmodium falciparum malaria in Laos. Herein, we aimed to study the efficacy of AL in the context of malaria elimination in Laos. Between Aug 1, 2019, and June 11, 2023, AL efficacy was evaluated in four provinces of southern Laos: Attapeu, Champassack, Salavan, and Savannakhet. Adults and children (aged 1-60 years) with microscopically confirmed P falciparum malaria received oral AL twice a day for 3 days, with follow-up on days 7, 14, 21, and 28. The primary outcome was PCR-adjusted adequate clinical and parasitological response (ACPR) by day 28. Resistance to dihydroartemisinin (DHA) and lumefantrine (LM) was assessed by an in vitro phenotypic analysis, and mutations in P falciparum kelch13 (pfkelch13), P falciparum multidrug resistance 1 (pfmdr1), P falciparum plasmepsin 2 (pfpm2), and P falciparum chloroquine resistant transporter (pfcrt) were characterised in parasites collected from enrolled patients. Safety outcomes included the frequency and nature of adverse events and serious adverse events. A total of 198 patients (median age 16 years [IQR 10-28]; 124 [63%] male and 74 [37%] female) were initially enrolled, of whom three were lost to follow-up, resulting in 195 patients who received the 3-day AL regimen. At day 28, the PCR-adjusted ACPR was 96% (95% CI 92-98), with a treatment failure rate of 2% (1-5) and a reinfection rate of 2% (1-5). Among the four PCR-confirmed recrudescent isolates, one showed markedly reduced LM susceptibility (LM 50% inhibitory concentration [IC50] 59·9 nM, 2·5 times higher than the median IC50 of other isolates) and high artemisinin resistance in vitro (ring-stage survival survival rate 35·8%), which was associated with the pfkelch13 R539T mutation and day-3 microscopy-positive parasitaemia. Among 190 isolates with successfully determined pfkelch13 sequencing, nine (5%) carried the pfkelch13 mutation R539T and 43 (23%) carried the C580Y mutation, and both were associated with day-3 microscopy-positive parasitaemia (p=0·044). No amplification of pfmdr1 or pfpm2, nor any mutations in pfmdr1 and pfcrt, were associated with treatment failure. Our findings indicate the potential emergence of LM resistance in Laos. Although AL remains efficacious, vigilance for decreasing efficacy and close monitoring of LM efficacy should be considered to support the country's goal of eliminating malaria by 2030. Importantly, none of the known pfmdr1 or pfcrt haplotypes were uniquely associated with treatment failure, including the isolate with the highest LM IC50, underscoring the need to identify reliable molecular markers for LM resistance. Bill and Melinda Gates Foundation and The Global Fund.

PMID 42155493
Read full article →

+8677 more articles available with a free account

Sign up free to view all articles →

Ask about artemisinin + amodiaquin