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artemisinin (artemisinin, Mateon / ArtiShield / ARTIVeda)

✓ Approved

Oncotelic Therapeutics, Inc. · therapeutic agent

What is artemisinin?

artemisinin is a therapeutic agent developed by Oncotelic Therapeutics, Inc.. It is approved for therapeutic indications via oral (po).

Drug Profile

Brand Namesartemisinin, Mateon, ArtiShield, ARTIVeda
CompanyOncotelic Therapeutics, Inc.
RouteOral (PO)
StatusApproved
Sources: ClinicalTrials.gov, Oncotelic Therapeutics, Inc.

Therapeutic Indications

artemisinin is developed for 6 unique indications across 6 therapeutic areas.

Therapeutic AreaConditionPhase
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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Related Research Articles

PubMedDose-response : a publication of International Hormesis Society2026-07-25

Mechanistic Insights Into Dose-Dependent Alleviation of Colorectal Cancer Through Artemisinin-Loaded Mesoporous Silica Nanoparticles in 1,2-Dimethylhydrazine-Induced Albino Wistar Rats.

Zahid Fatima F, Ilyas Umair U, Zahid Sara S, Gulzar Faisal F et al.

The current study investigates the suitability of encapsulating the Artemisinin-plant-originated lipophilic drug molecule into polyethylene glycol-coated mesoporous silica nanoparticles in a suitable dose regimen for the specific targeting of the drug in colorectal cancer. Mesoporous silica nanoparticles (MSNPs) were synthesized through the sol-gel method, and Artemisinin was loaded. Then characterization of Artemisinin-loaded mesoporous silica nanoparticles coated with polyethylene glycol (MSN-PEG@Artemisinin) was performed by Fourier transform infrared spectroscopy (FTIR), Zeta analysis, Polydispersity index (PDI) and X-Ray diffraction (XRD) techniques and compared with the standard drug Gemcitabine. The in vivo analysis of 1,2-dimethylhydrazine (DMH) was used to induce colorectal tumors in the colon of inbred male Wistar rats. The treatment group of rats was administered MSN-PEG@Artemisinin through intraperitoneal injection. Hematoxylin and eosin staining were performed to the histopathological examination of tumors. The average size of MSN-PEG@Artemisinin was 203.6 ± 64.78 nm with a zeta potential of -10.9mV. PDI was measured at 0.106. FTIR analysis also supported the successful loading of Artemisinin in mesoporous silica nanoparticles with PEG coating without showing interactions. The encapsulation efficiency (EE) and Drug loading (DL) percentages were 82.75% and 33.10%, respectively. XRD indicated a uniform mesoporous structure with a proper hexagonal symmetry. The in-vitro release was carried out in phosphate buffer with 7.4 pH following biphasic system with 26% drug release during the first 2.5 hours and 57% in 24 hours, indicating a good controlled release rate. In-vivo study revealed DMH-induced colorectal rats showed the increased tumor weight (34.8±0.75mg) tumor length (8.2±0.6) and tumor width (6.0±0.5) at a dose level of 0.5 ml/kg. Artemisinin loaded MSNPs significantly (p < .005) suppressed tumor weight (15.6±1.56), tumor length (5.7±0.23) and tumor width (2.3±0.8) at a dose level of 100 mg/kg body weight. Overexpression of 8-OHdG, MMP-7, CA-19-9, KRAS, IL-8, Caspase-8, PD-1 and PDL-1 in CRC, which were successfully treated with MSN-PEG@Artemisinin and standard Gemicitabine ((p≥0.056). MSNPs-PEG@Artemisinin suppressed DMH-induced colorectal carcinogenesis by targeting oxidative stress, KRAS/MMP-7/IL-8 inflammatory signaling, PD-1/PD-L1-mediated immune evasion, and Caspase-8-associated apoptotic dysregulation. These results highlight the potential of modified MSNPs as a versatile drug delivery system for colorectal cancer, providing a viable approach to enhance the therapeutic window of Artemisinin by controlling the dose while reducing the adverse effects of cancer therapies. This research contributes to advancements in pre-clinical studies and to improvements in targeted colorectal cancer therapies by providing insights into the development and use of mesoporous silica nanoparticles as a promising drug delivery system.

PMID 42500304
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PubMedFree radical biology & medicine2026-07-25

Physiologically relevant oxygen tensions reshape anticancer responses under oxidative stress-permissive culture conditions.

Mielczarek-Puta Magdalena M, Otto-Ślusarczyk Dagmara D, Żyżyńska-Granica Barbara B, Graboń Wojciech W et al.

Tumor hypoxia is a hallmark of solid malignancies and an important determinant of therapeutic response; however, most in vitro studies are still performed under atmospheric oxygen conditions that poorly reflect physiological tissue oxygenation. Conventional culture systems also rarely account for iron availability and polyunsaturated fatty acids (PUFAs), two important modulators of oxidative stress-associated cytotoxicity. This study investigated how physiologically relevant oxygen tension influences anticancer responses to oxidative stress-modulating compounds under iron- and PUFA-enriched conditions. Human colorectal, lung, and pancreatic cancer cell lines, together with non-tumorigenic HaCaT cells, were cultured under physioxic (10% O2) and hypoxic (1% O2) conditions in the presence of transferrin-bound iron and linoleic acid and exposed to artemisinin (ART), dihydroartemisinin (DHA), honokiol (HNK), and doxycycline (DOXY). The anticancer responses were strongly oxygen- and cell line-dependent. DHA exerted the strongest antiproliferative activity, inducing marked G0/G1 arrest and pronounced apoptosis, particularly under hypoxia. ART and HNK also displayed oxygen-dependent apoptotic and oxidative stress-associated effects, whereas DOXY primarily induced caspase activation accompanied by comparatively weak apoptosis. All compounds increased mitochondrial reactive oxygen species generation, while DHA and ART most consistently enhanced lipid peroxidation. In contrast, GPX4 protein expression remained largely unchanged in most cell lines, suggesting functional rather than expression-level modulation of ferroptosis-associated pathways. Collectively, these findings demonstrate that physiologically relevant oxygen tension profoundly reshapes anticancer responses to redox-active compounds and highlight the importance of incorporating physiologically relevant oxygen conditions into experimental cancer models.

PMID 42497949
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PubMedMedical oncology (Northwood, London, England)2026-07-24

A combination of artemisinin, moxidectin, and doxorubicin drugs can selectively and efficiently induce apoptosis in acute lymphoblastic and chronic myeloid leukemia cells in vitro and ex vivo.

Soto-Mercado Viviana V, Mendivil-Perez Miguel M, Jimenez-Del-Rio Marlene M, Velez-Pardo Carlos C

Acute lymphoblastic (ALL) and chronic myeloid (CML) leukemias are blood cancers that often resist traditional chemotherapy and other treatments. This is likely due to their ability to evade apoptosis. Therefore, inducing apoptosis in leukemia cells using innovative drug combinations may be the most effective therapeutic approach. Methods for multidrug combinations involving three or more drugs are scarce and much more complex to analyze. To address this issue, we propose an effective concentration 50 (EC50)-based, three-step method. The first step determines the lowest EC50 for each drug (e.g., artemisinin, chloroquine, primaquine, mefloquine, ivermectin, moxidectin, doxorubicin, and minocycline) by analyzing four cell endpoints (e.g., cell cycle, sub-G1, mitochondrial membrane potential (ΔΨm), autophagy (lysosomes), and cleaved caspase 3 (CC3)) on K562 cells. Step two involves establishing the deleterious effect of the EC50-based drug combination at concentrations of single drugs at 1-, ½-, and ¼-EC50, respectively, on K562 leukemia cells. Step three involves using the optimal combined drugs to evaluate the same cellular endpoints in other non-leukemic and leukemic cells. We found that the combination of AM (1 µM), MD (10 µM), and DR (1.5 µM), i.e., at ½ EC50, induced cell cycle arrest in the S (25% ± 13, N = 4) and G2/M (55% ± 18, N = 4) phases, a drastic loss of ΔΨm (81% ± 6, N = 4), high lysosome accumulation (82% ± 10, N = 4), and CC3 (83% ± 13, N = 4), as evidence of apoptosis in K562 and Jurkat cells and ex vivo ALL and CML cells. The combined drugs were innocuous to peripheral blood lymphocytes (PBLs) (S phase = 40%; G2/M = 26%; ΔΨm = 4%; lysosomes = 3%; CC3 = 4%; n = 3). Our approach to combining drugs has the potential to provide a new pharmacological treatment for leukemias.

PMID 42496777
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PubMedChemMedChem2026-07-24

Aminopeptidase Inhibition in Drug-Resistant Plasmodium falciparum: Structural, Functional, and Pharmacological Rationale for Targeting PfA-M1 and PfA-M17.

Lim Sharoen Yu Ming SYM

Malaria remains a significant global health burden, increasingly threatened by the emergence of artemisinin-resistant Plasmodium falciparum strains that compromise the efficacy of frontline combination therapies. Hemoglobin digestion constitutes a central metabolic pathway sustaining intraerythrocytic parasite growth, in which the terminal processing of hemoglobin-derived peptides and liberation of free amino acids are mediated by two zinc-dependent metalloaminopeptidases, PfA-M1 (M1 alanyl aminopeptidase) and PfA-M17 (M17 leucyl aminopeptidase). This review synthesizes current evidence supporting PfA-M17 and PfA-M1 as validated antimalarial targets, with particular emphasis on the structural biology, catalytic regulation, and cellular essentiality of PfA-M17. We discuss how the oligomerization-dependent activation of PfA-M17, governed by metal-ion-mediated quaternary assembly and a dynamic regulatory loop (L13), imposes structural constraints that may limit resistance evolution. We further evaluate selective and dual-target inhibitors, including MMV1557817 and compound 26, that demonstrate cross-species antiplasmodial efficacy with substantial fitness costs on resistant parasites. The mechanistic interplay between aminopeptidase inhibition and established antimalarial drug classes, including quinolines and artemisinins, is also examined. This review supports dual PfA-M1/PfA-M17 inhibition as a promising approach for next-generation antimalarial drug development.

PMID 42493361
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PubMedBioorganic & medicinal chemistry letters2026-07-23

Conversion of artemisinin into novel unprotected N-alkylamine-11-azaartemisinins with enhanced antimalarial activity.

Rathi Komal K, Gupta Aashima A, Yadav Priyanka P, Rawat Varun V et al.

Two novel azaartemisinin scaffolds N-ethanamine-11-azaartemisinin (EAZA) 10 and N-propanamine-11-azaartemisinin (PAZA) 11 were synthesized from artemisinin 1 on multigram scale in excellent yields without the need for further column chromatography purification and evaluated for their in vitro antimalarial potential. Relative to artemisinin (IC₅₀ = 6.978 nM), EAZA (IC₅₀ = 1.43 nM) and PAZA (IC₅₀ = 144.4 pM) exhibited approximately 3.5-fold and 30-fold greater antimalarial potency, respectively, while maintaining low cytotoxicity toward HepG2 cells, as indicated by their high cytotoxic concentration values. Thermogravimetric Analysis (TGA), isothermal titration calorimetry (ITC), and density functional theory (DFT) provided insights into their structure-property relationships. This study highlights the profound impact of minimal structural variations on the biological and thermal properties of azaartemisinins.

PMID 42486375
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PubMedIranian journal of pharmaceutical research : IJPR2026-07-23

Tehranolide Attenuates Lipid Accumulation in Steatotic HepG2 Cells via cAMP/AMPK/SIRT1-Mediated Autophagy Activation.

Lorestani Shima S, Mohammad Ganji Shahla S, Noori Shokoofe S

Metabolic dysfunction-associated steatotic liver disease (MASLD) is a prevalent metabolic condition marked by abnormal lipid buildup within hepatocytes, leading to inflammation and liver injury. Hepatic lipid accumulation can be driven by multiple factors, including high glucose, free fatty acids, and lipotoxic stress. Autophagy, which may be influenced by metabolic regulators such as cyclic adenosine monophosphate (cAMP), AMP-activated protein kinase (AMPK), and sirtuin 1 (SIRT1), is suggested to contribute to the maintenance of hepatic lipid homeostasis. Tehranolide, a sesquiterpene lactone derived from Artemisia diffusa and structurally related to artemisinin, is believed to have hepatoprotective effects similar to artemisinin. This work is the first to assess the impact of tehranolide on lipid accumulation with emphasis on autophagy/AMPK/SIRT1 signaling in steatotic human hepatoma-derived cells (HepG2). This investigation was undertaken to evaluate the potential of tehranolide to reduce lipid accumulation in a high-glucose-induced steatotic hepatocyte model, potentially involving autophagy-related signaling pathways such as cAMP, AMPK, and SIRT1. A high-glucose-induced steatotic model was established in HepG2 cells. After determining the effective concentration of tehranolide by means of the MTT assay, lipid-loaded cells received treatment with tehranolide. The content of intracellular triglycerides (TGs) was determined via Oil Red O staining and commercial kits. The expression of lipid metabolism-related genes [fatty acid synthase (FASN), sterol regulatory element-binding protein 1c (SREBP-1c), and SIRT1] and autophagy markers [light chain 3 (LC3), beclin-1] was analyzed by quantitative real-time polymerase chain reaction (qRT-PCR), while protein levels of LC3-I, LC3-II, AMPK, and phosphorylated AMP-activated protein kinase (p-AMPK) were evaluated by Western blotting. Intracellular cAMP levels, lactate dehydrogenase (LDH) release, and inflammatory cytokines were also quantified using commercial kits. Tehranolide significantly decreased intracellular TG levels, downregulated lipogenic genes (FASN, SREBP-1c), and upregulated the lipolytic gene SIRT1. It increased the expression of autophagy-related markers (beclin-1 and LC3-II). Furthermore, tehranolide increased intracellular cAMP and AMPK phosphorylation, while inhibition of SIRT1 or blockade of autophagy attenuated these effects. In addition, tehranolide reduced glucose-induced cytotoxicity and suppressed pro-inflammatory cytokine production in HepG2 cells. Tehranolide attenuates lipid accumulation and inflammatory responses in high-glucose-induced steatotic HepG2 cells, potentially involving autophagy-related processes, which may be linked to cAMP, AMPK, and SIRT1. These findings suggest that tehranolide may represent a potential modulator of hepatocellular lipid metabolism in glucose-induced steatosis, warranting further validation in more comprehensive in vitro and in vivo models.

PMID 42488761
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