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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

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

PubMedMolecular medicine reports2026-09-18

Artemisinin and its derivatives for metabolic syndrome: From multi‑target mechanisms to translational opportunities (Review).

Cao Shuo S, Yang Mo M, Qu Siyu S, Wu Jinsong J et al.

Metabolic syndrome (MetS) is a complex of disorders, characterized by insulin resistance accompanied by abdominal obesity, dyslipidemia, hypertension and impaired glucose metabolism. This group of conditions notably increases the risk of type 2 diabetes mellitus and cardiovascular or cerebrovascular diseases and has become a major global public health challenge. Current treatments for MetS often fail to meet clinical needs owing to the limitations associated with single‑target therapies and notable side effects. Artemisinin‑based drugs are primarily used as antimalarial drugs but have garnered widespread attention for their broad biological activities. Preclinical evidence suggests that artemisinin and its derivatives improve insulin sensitivity, regulate lipid metabolism, alleviate chronic inflammation and reshape the gut microbiota by modulating multiple metabolism‑related signaling pathways, including AMP‑activated protein kinase, PI3K/Akt, NF‑κB and Toll‑like receptor 4, indicating a potential therapeutic avenue for MetS. However, most of these findings are derived from cell‑based and animal studies, while direct clinical evidence in patients with MetS remains limited. In the present review, the therapeutic potential and core molecular mechanisms of artemisinin and its derivatives for MetS are summarized and the challenges and opportunities for their future clinical translation are discussed.

PubMedOrganic & biomolecular chemistry2026-09-18

Inter- and intramolecular photoactivation of artemisinin and derivatives by xanthone-based triplet and singlet sensitizers.

van Stiphoudt Jan F W JFW, Bold Christina C, Griesbeck Axel G AG

Molecular dyads and triads were synthesised using mono- and diaminoxanthones as chromophores and artesunate as a pharmacophore. During photolysis, non-fluorescent xanthone as well as the fluorescent aminoxanthone hybrids ART-XO and (ART)2-XO underwent peroxide rearrangement, resulting in quenching of fluorescence alongside peroxide decomposition. The most probable pathway involves O-O-bond activation through singlet and triplet energy transfer (en-T). The activation of artemisinin by xanthone is due to intermolecular triplet en-T, which leads to two characteristic peroxide rearrangement products.

PubMedScientific reports2026-09-16

Specific targeting of cancer cell mitochondria with a malaria drug improves pancreatic cancer outcome.

Ou Yan Y, Lim Adrian A, Wang Ruoxiang R, Mir Nora N et al.

Pancreatic ductal adenocarcinoma (PDAC) is a lethal malignancy. In this paper, we present DZ-ART1, a first-in-class, dual-function therapeutic. This innovative agent is composed of a tumor-targeting heptamethine carbocyanine dye conjugated to artemisinin (ART). Near-infrared imaging demonstrated precise tumor localization of DZ-ART1 in mice. DZ-ART1 accumulated 5- to 10-fold more in cancer cells compared to normal cells. DZ-ART1 significantly decreased the survival of eight PDAC cell lines with little effect on normal cells. It increased the lethal effect of chemotherapies in vitro and in vivo. Functional assays confirmed DZ-ART1's ability to disrupt mitochondrial bioenergetics, deplete ATP, and induce reactive oxygen species production. Mitochondrial depletion of cancer cells decreased DZ-ART1 uptake and cytotoxicity, highlighting its mechanistically unique, mitochondria-dependent action. Transcriptomic profiling revealed DZ-ART1's broad reprogramming of PDAC pathways related to cell survival, cancer stemness, and metastasis. In three rigorously validated preclinical models - Krasþ/LSLG12D;Trp53þ/LSLR172H;Pdx-1-Cre (KPC) transgenic, syngeneic, and patient-derived xenografts (PDX) - DZ-ART1 markedly suppressed tumor growth and metastasis and prolonged survival, all without toxicity to normal tissues. DZ-ART1 represents a new class of anti-cancer therapeutics that uniquely combines diagnostic imaging and cancer cell organelle-specific targeting.

PubMedBioorganic chemistry2026-09-16

Design, synthesis and biological evaluation of novel artesunate-selenylindole hybrids against colorectal cancer.

Cao Jianlong J, Yuan Ge G, Li Changgui C, Ren Meilin M et al.

Colorectal cancer (CRC) remains a major global public health threat, creating an urgent demand for novel therapeutic agents. Artesunate (ART), a semisynthetic derivative of artemisinin, has demonstrated anti-colorectal cancer effects, but its moderate antitumor potency (IC50 > 50 μM) severely limits further clinical application. To enhance the activity against colorectal cancer (CRC), we adopted a scaffold hybridization strategy to rationally design and synthesize 22 novel artesunate-selenylindole hybrids. All derivatives were screened for their anti-proliferative activity against four human colorectal cancer cell lines (HT29, HCT116, SW480, SW620) and normal human liver cells (LO2). Most derivatives exhibited superior anti-proliferative activity compared to ART (IC50 > 50 μM), and compound 3e demonstrated significant anti-proliferative activity against HCT-116 cells with an IC50 of 6.0 μM and exhibiting no toxicity toward normal cells. Further cellular assays verified that 3e suppresses colony formation and cell migration of HCT116 in a dose-dependent fashion. Mechanistically, 3e inhibits TrxR activity to trigger intracellular ROS overaccumulation and mitochondrial dysfunction. The accumulated oxidative stress elicits G0/G1 cell-cycle arrest and pronounced mitochondrial-dependent apoptosis, characterized by elevated Bax, cleaved-caspase-3, cleaved-PARP, reduced Bcl-2 and procaspase-3, and the release of cytochrome-c from mitochondria to cytoplasm. In summary, compound 3e displays potent anti-CRC effects through TrxR/ROS-driven oxidative-stress signaling, representing an attractive lead scaffold for anti-CRC drug discovery.

PubMedJournal of clinical medicine2026-09-15

Advanced Biological Therapies: Principles, Mechanisms and Medical Applications.

Brozek Rafal R, Lorenz Antonina A, Dorocka-Bobkowska Barbara B, Kurpisz Maciej M

Biotherapeutics are medicinal agents derived from or related to naturally occurring molecules in the body and are designed to modulate specific immune targets. This review examines clinically established biologics and targeted small molecules that affect cytokine-driven transcriptional programs, principally JAK/STAT and canonical and non-canonical NF-κB signaling, across autoimmune, neoplastic, hematological, dermatological, and rheumatic diseases. Periodontitis is used as a translational model because dysbiotic mucosal inflammation, cytokine signaling, and osteoclastogenesis may also intersect with systemic autoimmunity. In particular, Porphyromonas gingivalis-associated protein citrullination provides a plausible link to anti-citrullinated protein antibody-positive rheumatoid arthritis in genetically susceptible individuals, although causality remains unproven. The review also evaluates plant-derived modulators of JAK/STAT and related transcriptional pathways. Curcumin and resveratrol have entered small rheumatoid arthritis studies, whereas evidence for catechins, celastrol, and artemisinin derivatives in autoimmune disease remains predominantly preclinical. These compounds may inform adjunctive or locally delivered strategies, but clinical translation requires better target selectivity, bioavailability, dose standardization, and safety data.

PubMedInternational journal of molecular sciences2026-09-15

Antiplasmodial Compounds from Eurycoma harmandiana Pierre and Eurycoma longifolia Jack Against Drug-Resistant Plasmodium falciparum: An Integrated In Vitro and In Silico Study.

Konyanee Atthaphon A, Wahab Habibah A HA, Kamarulzaman Ezatul Ezleen EE, Suhaimi Ahmad Marwazi Mohd AMM et al.

Malaria is a life-threatening global disease, and despite artemisinin-based combination therapies (ACTs) as first-line treatment, emerging drug-resistant Plasmodium strains necessitate novel antimalarial agents. This study investigated the antiplasmodial potential of Eurycoma harmandiana Pierre (EH) root extract, a medicinal plant closely related to Eurycoma longifolia Jack (EL). The extract and its derived compounds were evaluated using in vitro antiplasmodial and cytotoxicity assays. The active compounds were further investigated by parasite morphological analysis, molecular docking against quadruple-mutant Plasmodium falciparum dihydrofolate reductase (qmPfDHFR), molecular dynamics (MD) simulations, and in silico prediction of drug-likeness, pharmacokinetic properties, and toxicity. The ethanolic extract exhibited potent antiplasmodial activity (IC50 = 0.51 µg/mL) with low cytotoxicity (CC50 = 31.68 µg/mL) and a high selectivity index (SI = 62.11). Quassinoids showed the strongest activity (IC50 = 0.13-0.87 µM), whereas alkaloids displayed good to moderate activity. The extract and two promising bioactive quassinoids, eurycomanone (1) and glaucarubolone (5), disrupted intraerythrocytic parasite development. Molecular docking and MD simulations demonstrated that glaucarubolone (5) exhibited favorable predicted interactions with qmPfDHFR, along with favorable predicted drug-like properties, pharmacokinetic profiles, and low toxicity. This study provides the first report of the antiplasmodial activity of Eurycoma harmandiana, highlighting it as a promising alternative source of bioactive compounds against Plasmodium parasites. Glaucarubolone (5) may represent a promising scaffold for further investigation toward the development of novel antimalarial agents.

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