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doxorubicin (doxorubicin, Nanox / Doxonax)

✓ Approved

Nanox · TOP2A · Small Molecule

What is doxorubicin?

doxorubicin is a small molecule developed by Nanox. It is approved for therapeutic indications via injectable (others).

Drug Profile

Brand Namesdoxorubicin, Nanox, Doxonax
CompanyNanox
Drug ClassSmall Molecule
Molecular TargetTOP2A
RouteInjectable (Others)
StatusApproved
Sources: ClinicalTrials.gov, Nanox

Mechanism of Action

Molecular Targets

doxorubicin acts on 1 molecular target:

TOP2ADNA topoisomerase II alpha (TOP2alpha, TOPIIA)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

doxorubicin is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Kaposi's sarcoma✓ Approved

Related Research Articles

PubMedBritish journal of pharmacology2026-07-25

sGC stimulator BAY 41-8543 improves survival and ventricular function in a rat model of doxorubicin-induced cardiomyopathy with nephrotic syndrome.

Gawrys Olga O, Škaroupková Petra P, Kikerlová Soňa S, Vaňourková Zdeňka Z et al.

Anthracyclines such as doxorubicin (DOXO) remain a cornerstone of cancer therapy but are associated with a high risk of cardiotoxicity and subsequent heart failure (HF). Impairment of NO/soluble guanylyl cyclase (sGC)/cGMP pathway has been reported in anthracycline-induced cardiomyopathy. This raises the hypothesis that increasing cGMP by sGC stimulation could preserve cardiac function even after HF has developed. This study aimed to evaluate the long-term effects of treatment with sGC stimulator BAY 41-8543 in a model of DOXO-induced HF with nephrotic syndrome in hypertensive rats. Male Ren-2 transgenic rats received five weekly intravenous injections of DOXO (cumulative dose 10 mg·kg-1) to induce cardiomyopathy. After two additional weeks, animals were treated with either BAY 41-8543 (10 mg·kg-1·day-1) or an ACE inhibitor (ACEi; trandolapril, 0.25 mg·kg-1·day-1). Echocardiography, blood and urine collection were performed at baseline (week -1) and 4 weeks after the treatment started to assess cardiac ventricular function, cardiac and renal biomarkers; survival at 20 weeks. Treatment with BAY 41-8543 improved long-term survival, preserved left and right ventricular systolic function and reduced myocardial expression of inflammation-related genes, particularly those linked to type I interferon signalling. ACEi provided stronger benefits in survival and structural remodelling. Kidney damage and function was not improved by any treatment compared to placebo. The sGC stimulator BAY 41-8543 exerted significant cardioprotective effects in DOXO-induced HF. Therefore, sGC stimulators may represent a promising therapeutic option for anthracycline-induced cardiomyopathy, although additional studies are required to fully investigate their therapeutic potential.

PMID 42498692
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PubMedJournal of controlled release : official journal of the Controlled Release Society2026-07-25

Tumor-targeted CD40 ligand-functionalized extracellular vesicle mimetics enable chemoimmunotherapy for neuroblastoma.

Wang Jinkui J, Luo Junyi J, Li Jiahui J, Zhang Zhaoxia Z et al.

Neuroblastoma remains one of the most lethal pediatric solid tumors, and durable control of high-risk disease is hindered not only by inefficient tumor-selective drug delivery but also by a profoundly immunosuppressive tumor microenvironment. To address these dual barriers, we developed a chemoimmunotherapeutic vesicle-mimetic platform, DAS/CD40L-EM@DOX, by engineering CD40L-overexpressing HEK-293 T donor cells, generating extracellular vesicle mimetics through extrusion, decorating the membrane with a neuroblastoma-targeting DAS peptide, and post-loading doxorubicin. The resulting formulation preserved a nanoscale vesicular morphology, displayed CD40L on the membrane, and showed favorable particle size and zeta potential characteristics. In neuroblastoma cells, DAS decoration enhanced uptake in an α7 nicotinic acetylcholine receptor-associated manner and increased the cytotoxic and immunogenic effects of doxorubicin, as evidenced by augmented apoptosis, calreticulin exposure, and HMGB1 release. In macrophage assays, CD40L-containing vesicles shifted M2-like cells toward an M1-like phenotype, increasing CD86, TNF-α and IL-6 while decreasing CD206, IL-10 and TGF-β. Functionally, this repolarization enhanced tumor-cell phagocytosis and promoted CD8+ T-cell effector responses, including increased granzyme B, IFN-γ and IL-2 production. In tumor-bearing mice, DAS modification improved tumor accumulation and reduced off-target sequestration relative to unmodified vesicles. Therapeutically, DAS/CD40L-EM@DOX exerted the strongest inhibition of tumor growth, reduced tumor burden, prolonged survival, increased intratumoural M1-like macrophages and CD8+ T cells, decreased M2-like macrophages and regulatory T cells, and enhanced immunogenic cell-death markers in situ. Together, these findings support DAS/CD40L-EM@DOX as a dual-function vesicle-mimetic nanomedicine that couples neuroblastoma-targeted chemotherapy with macrophage reprogramming to remodel the tumor immune microenvironment and improve antitumour efficacy.

PMID 42498231
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PubMedBiosensors & bioelectronics2026-07-25

Fast-scan voltammetry with an ultramicroelectrode for single-cell monitoring of DNA damage: Drug evaluation and chiral nanomaterial toxicity assessment.

Zhou Huiqian H, Guo Yuxin Y, Long Lifen L, Wang Shuihua S et al.

DNA integrity is essential for cellular function and chemotherapy response, but real-time, single-cell monitoring of DNA damage has been difficult to achieve. In this study, we constructed an electrochemical biosensor using a DNA-modified platinum nanoelectrode (PtNE/DNA) combined with fast-scan voltammetry (FSV) at 30 kV s-1 for dynamic detection of DNA damage in a single living cell. The sensing platform utilizes a ferrocene-labeled hairpin DNA probe that specifically recognizes structural damage, while the high temporal resolution and strong anti-interference capability are provided by the FSV technology. We successfully monitored real-time DNA damage in a single HeLa cell treated with chemotherapeutic agents including doxorubicin (DOX), cisplatin (CDDP), and paclitaxel (PTX). Distinct kinetic profiles were observed: DOX elicited the most rapid and severe damage, CDDP induced intermediate progression, and PTX resulted in delayed and attenuated effects. Furthermore, we revealed enantioselective cytotoxicity of chiral carbon dots (D-CDs and L-CDs), with L-CDs showing significantly higher toxicity. These results demonstrate the utility of our approach in assessing drug sensitivity and nanomaterial biocompatibility at the single-cell level, providing a valuable tool for advancing precision medicine and toxicological research.

PMID 42497549
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PubMedActa naturae2026-07-25

Senolytic Properties of DR5-Selective TRAIL in Pancreatic Cancer Cell Lines.

Isakova A A AA, Antipova N V NV, Mazur D V DV, Ivanova E I EI et al.

Pancreatic adenocarcinoma is one of the most aggressive cancers. Its treatment relies on conventional chemotherapy agents; particularly gemcitabine. Chemotherapy is known to induce cell cycle arrest and the development of a senescent phenotype in tumor cells. The accumulation of senescent cells limits tumor proliferation, followed by the secretion of factors of the senescence-associated secretory phenotype promoting malignancy in the tumor microenvironment and metastasis. This makes the search for drugs suitable for senolytic therapy highly relevant. This study explored the senolytic properties of a DR5 receptor-selective mutant variant of the antitumor cytokine TRAIL DR5-B in human pancreatic cancer cell lines, after prolonged co-incubation with gemcitabine or doxorubicin. In the MIA PaCa-2 and PANC-1 cell lines, both drugs significantly increased β-galactosidase activity and the expression of senescence markers, such as the cell cycle inhibitors p21 and p27; DR5-B effectively suppressed cell viability after chemotherapy treatment. In the BxPC-3 cell line, the drugs did not induce senescence and DR5-B cytotoxicity was virtually unchanged. Some features of senescence were observed in AsPC-1 cells; however, these cells remained resistant to DR5-B, presumably due to cFLIP overexpression. Hence, the DR5-B protein shows promise as a senolytic agent for the treatment of certain types of pancreatic adenocarcinoma.

PMID 42499672
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PubMedFrontiers in oncology2026-07-25

Therapeutic assessment of Nerium oleander-derived exosome-like nanoparticles against triple-negative breast cancer: a preliminary in vitro and network pharmacology approach.

Routh Sreyoshi S, Joseph Tomsy T, Sreekumar Arya A, Manickam Venkatraman V

Triple-negative breast cancer (TNBC) is an aggressive subtype lacking estrogen, progesterone, and HER2 receptors, which restricts targeted therapies and contributes to poor survival. Conventional chemotherapeutics such as doxorubicin and cisplatin show limited efficacy, significant toxicity, and resistance, underscoring the need for alternative strategies. Nerium oleander, a traditional medicinal plant, has demonstrated anticancer activity through leaf extracts; however, the role of exosome-like nanoparticles derived from its flowers (NELNs) remains unexplored. The therapeutic efficacy of NELNs was evaluated in the MDA-MB-231 TNBC cell line using in vitro and in silico approaches. Cytotoxicity was assessed by the MTT assay, while AO/EtBr and DCFDA staining examined apoptosis and ROS generation through fluorescence microscopy. Flow cytometry was employed for apoptosis confirmation and cell cycle analysis. Network pharmacology integrating target prediction, PPI network construction, and functional enrichment analysis was performed, followed by molecular docking of NELN-encapsulated metabolites against predicted targets. NELNs induced significant cytotoxicity, promoted apoptosis, and increased intracellular ROS levels in MDA-MB-231 cells. Flow cytometry confirmed apoptotic induction and revealed alterations in cell cycle progression. Pathway enrichment analysis of previously identified NELN-associated metabolites computationally highlighted arachidonic acid and linoleic acid metabolism, with cytochrome P450 enzymes (CYP1A2, CYP2C9, CYP3A4) emerging as putative targets. Molecular docking predicted favorable binding interactions of NELN metabolites to these targets. This study provides preliminary evidence that flower-derived NELNs exerted antiproliferative and pro-apoptotic activity against MDA-MB-231 cells under the tested experimental conditions. Furthermore, network pharmacology analyses generated putative mechanistic insights into pathways relevant to TNBC.

PMID 42500301
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PubMedCellular signalling2026-07-25

Impaired mitochondrial quality control and stress signalling machinery modulate senescence induction by genotoxic challenge.

Weston Mia Simons MS, Prieto Marta Dominguez MD, Moisoi Nicoleta N

Cellular senescence is a hallmark of ageing and age-related disease and is closely associated with mitochondrial dysfunction and the accumulation of DNA damage. However, the contribution of mitochondria-nucleus communication, mitochondrial quality control (mtQC) and stress signalling to senescence remains incompletely understood. Here, we investigated the interplay between mtQC pathways and cellular stress responses in DNA damage-induced senescence using mouse embryonic fibroblasts (MEFs). MEFs deficient in the mitochondrial protease HtrA2 (proteostasis), the transcription factor Chop (integrated stress response; ISR) or the mitophagy regulator Pink1 were exposed to three mechanistically distinct DNA-damaging agents: bleomycin, etoposide and doxorubicin. Senescence was characterised using multiple complementary markers, including the proportion of high senescence-associated β-galactosidase-positive cells, nuclear size, total and nuclear p21 abundance, and transcriptional analysis of p16, p21 and genes associated with cell-cycle regulation and stress signalling. Mitochondrial dysfunction through mtQC impairment enhanced sensitivity to senescence with HtrA2 and Pink1 loss promoting increased senescence under DNA damage. Although DNA damage response (DDR) was activated as seen by changes in p21 homeostasis, this did not always correlate with senescence levels, which indicates that DDR alone cannot account for all senescence characteristics. The ISR played a modulatory role in the senescence induction, with Chop loss of function reducing senescence induction following DNA damage despite DDR activation. The different DNA damaging drugs produced different senescence outcomes, thus highlighting the importance of the stressor context in addition to the cellular homeostasis mechanisms in the overall senescence profile. This approach allowed, for the first time, to identify senescence subtypes dependent of mtQC and ISR integrity in the context of genotoxic stress.

PMID 42498093
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