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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

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PubMedFuture medicinal chemistry2026-11-12

Design, synthesis, and mechanistic elucidation of lawsone derivatives as novel inducers of ROS-associated mitochondrial apoptosis in breast cancer.

Hassan Aisha Y AY, Abou-Amra Eman S ES, El Saeed Hoda S HS, El-Sebaey Samiha A SA et al.

Novel monomeric and dimeric lawsone derivatives were designed and investigated for their cytotoxicity. Lawsone derivatives (2-8) were synthesized under solvent-free conditions and tested against MDA-MB-231 and MCF-7 breast cancer cells versus doxorubicin. Mechanistic studies included reactive oxygen species (ROS) generation, mitochondrial membrane potential (ΔΨm), cell-cycle distribution, apoptosis, and apoptosis-related genes. Dimeric derivatives 7 and 8 exhibited the highest cytotoxicity, particularly against MDA-MB-231 cells, with half-maximal inhibitory concentration (IC50 values of 0.37 and 1.43 µg/mL, respectively, outperforming doxorubicin (16.3 µg/mL). Both compounds showed high selectivity for MDA-MB-231 cells relative to WI-38 fibroblasts (selectivity index (SI) = 59.5 and 28.2, respectively). Mechanistic investigations demonstrated that compounds 7 and 8 induced significant ROS-related signals, associated with ΔΨm disruption. Concurrently, they induced gap 0/gap 1 (G0/G1) phase cell cycle arrest and promoted apoptosis with minimal necrosis. Compound 7 significantly upregulated Bcl-2-associated X protein (Bax) (6.6-fold) and caspase-9 (8.0-fold) while downregulating B-cell lymphoma 2 (Bcl-2) and poly (ADP-ribose) polymerase 1 (PARP-1), supporting activation of the intrinsic mitochondrial apoptotic pathway. Dimerization substantially enhanced the anticancer potency and selectivity of the lawsone scaffold. Compounds 7 and 8 represent promising lead structures for further optimization and development of potent anticancer agents.

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PubMedDrug metabolism and bioanalysis2026-11-12

Docking Studies of Punica granatum Metabolites: A Pathway toward Novel Anti-Cancer Therapeutics.

Gavate Deepak P DP, Badgujar Vilas L VL, Shirole Nitin L NL, Shirole Rahul L RL et al.

Cancer is a major global health challenge, and the search for new, more effective treatments with reduced toxicity is ongoing. Natural compounds from plants, such as those found in Punica granatum (pomegranate), have shown promise as potential anticancer agents. However, to date, no scientific molecular docking studies have been reported that elucidated the mechanism of action of these metabolites. Molecular docking is a method used to evaluate how well three key compounds from Punica granatum-ellagic acid, punicalagin, and punicalin-bind to the TRIM24 PHDbromodomain protein, a target known to play a role in cancer progression. The docking results indicated that punicalagin demonstrated the highest binding affinity (-8.5 kcal/mol), succeeded by punicallin (-7.8 kcal/mol) and ellagic acid (-6.9 kcal/mol). Both punicalagin and punicalin exhibited enhanced binding interactions relative to methotrexate (-7.4 kcal/mol) and doxorubicin (-7.1 kcal/mol). The study found that Punica granatum metabolites, particularly punicalagin, bind the TRIM24 PHDbromodomain protein best. Punicallin and ellagic acid had higher binding affinities than methotrexate and doxorubicin, two common chemotherapeutics. Therefore, Punica granatum metabolites may be a better and safer alternative to conventional chemotherapy agents, which have many side effects. The findings indicated that metabolites of Punica granatum, particularly punicalagin, may serve as potent anticancer agents capable of inhibiting cancer-associated targets such as TRIM24. This facilitates more inquiry into pharmaceutical development.

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PubMedCell & bioscience2026-11-12

Recombinant GDF15 prophylaxis attenuates cardiorenal toxicity and fibrosis induced by doxorubicin and angiotensin II.

Fung Erik E, Luo Hangqi H, Chen Jack C H JCH, Zhu Wenjuan W et al.

Anthracycline chemotherapy induces cardiotoxicity through mitochondrial damage and cell apoptosis that are exacerbated in vivo by angiotensin II (Ang II). Growth differentiation factor 15 (GDF15) is a stress-responsive cytokine with protective functions but its capacity to mitigate doxorubicin (Dox)-induced cardiotoxicity and Ang II-associated cardiorenal stress remains unclear. Human embryonic stem cell-derived cardiomyocytes were used to evaluate Dox toxicity and to benchmark recombinant GDF15 against conventional dexrazoxane pretreatment. Cardiomyocyte viability, mitochondrial integrity and function, apoptosis, and transcriptome profiles by RNA sequencing were evaluated. To determine in vivo efficacy, C57BL/6 J mice were administered GDF15 (0.5 mg/kg, intraperitoneal) 24 h before once weekly Dox (5 mg/kg). Ang II was infused subcutaneously via surgically implanted osmotic pump. Mice were sacrificed for histopathologic analysis 1 week after the fourth cycle of Dox. In vitro, Dox-induced mitochondrial fragmentation, loss of membrane potential, transcriptional dysregulation, and apoptosis were significantly attenuated by recombinant GDF15 pretreatment, with efficacy comparable to dexrazoxane. Cytotoxic effects of daunorubicin on cardiomyocytes were also attenuated by GDF15. In vivo, Ang II, Dox, and Dox + Ang II induced cardiorenal injury characterized by hypertension, sarcomere disarray, myocardial and renal fibrosis, and glomerular, tubular, and perivascular abnormalities. GDF15 prophylaxis mitigated these pathologic changes, preserved myocardial and renal tissue architecture, and reduced cardiorenal fibrosis. Recombinant GDF15 pretreatment can protect the heart and kidneys from Dox-induced cardiorenal toxicity and Ang II-exacerbated injury. These findings encourage further investigation into GDF15 as a potential prophylaxis against cardiorenal toxicity associated with anthracycline chemotherapy and renin-angiotensin system activation.

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High-Pressure/High-Dose Versus Standard PIPAC in Epithelioid Peritoneal Mesothelioma: Safety, Feasibility, and Outcomes From a Bicentric Comparative Cohort Study.

Kockelmann Fabian F, Michot Nicolas N, Demtröder Cédric R D CRD, Schmeding Maximilian M et al.

Pressurized intraperitoneal aerosol chemotherapy (PIPAC) is a minimally invasive option for peritoneal mesothelioma (PeM) in patients not eligible for cytoreductive surgery (CRS) and hyperthermic intraperitoneal chemotherapy (HIPEC). This bicentric study compared the safety, feasibility, and sex-specific outcomes of standard versus high-pressure/high-dose PIPAC (HP/HD-PIPAC). Patients who had non-resectable epithelioid PeM (ePeM) treated with PIPAC at two German centers were retrospectively analyzed. Group 1 received standard PIPAC (cisplatin 7.5 mg/m2 + doxorubicin 1.5 mg/m2, 12 mmHg), and group 2 received HP/HD-PIPAC (cisplatin 20 mg/m2 + doxorubicin 4 mg/m2, 20 mmHg). Procedural outcomes, postoperative complications, interval from diagnosis to first PIPAC, and overall survival (OS) were analyzed. Uni- and multivariable Cox regression analyses were performed to identify factors associated with OS. The 46 patients in the study (group 1: 25 patients; group 2: 21 patients) underwent 120 of 132 scheduled PIPAC procedures. The median OS from diagnosis was 48 months overall: 48 months in group 1, and 36 months in group 2. The interval from diagnosis to first PIPAC was shorter in group 2 (2 vs. 20 months; p = 0.009). Severe complications (Clavien-Dindo ≥III) occurred in 6.2 % of group 1 versus 2.9 % of group 2. The median OS was 106 months for the females versus 35 months for the males (p = 0.064). Multivariable analysis identified female sex, bidirectional treatment, and a longer interval between diagnosis and first PIPAC as independent factors associated with improved OS. The HP/HD-PIPAC regimen is feasible and safe. Although no significant survival differences were observed between treatment groups, prospective studies are required to define the optimal timing and integration of PIPAC within multimodal treatment strategies. Findings should be interpreted in the context of the retrospective study design.

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PubMedJournal of medicinal chemistry2026-11-12

Modular Biomimetic Strategy toward Discovery of Macrocyclic Sulfonamides as SIRT3 Activators against Heart Failure.

Yang Xiaoxiao X, Liu Simin S, Cui Yunxia Y, Liu Hepeng H et al.

Heart failure (HF) remains a severe global cardiovascular disease with limited targeted therapies. Mitochondrial deacetylase SIRT3 is a promising therapeutic target for HF, yet current SIRT3 agonists suffer from low potency and poor isoform selectivity. Herein, we adopted a modular biomimetic strategy to synthesize a series of macrocyclic sulfonamides and systematically explored their structure-activity relationships. The lead compound 2b (Y0855) exhibited potent SIRT3 agonistic activity (EC50 = 12.6 μM, and Emax = 4.05) and excellent selectivity over SIRT1/2/6. Mechanistically, 2b alleviated cardiomyocyte oxidative stress, cell injury and fibrosis via SIRT3 activation. In a doxorubicin-induced HF mouse model, it markedly restored cardiac function and mitigated myocardial damage. Moreover, 2b possessed improved metabolic stability, making it a valuable lead compound for anti-HF drug development targeting SIRT3.

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PubMedRSC advances2026-11-12

Discovery of novel 1,3,4-thiadiazole derivatives as potential dual EGFR/VEGFR inhibitors with activity against breast, colon, and liver cancer cells: biological evaluation and molecular docking investigation.

Belal Amany A, Abourehab Mohammed A S MAS, Alsantali Reem I RI, Obaidullah Ahmad J AJ et al.

New derivatives of the 1,3,4-thiadiazole scaffold were synthesized and evaluated for their cytotoxic effects on breast (MCF-7), hepatic (HepG-2), and colorectal (HCT-116) carcinomas. The most active compounds (7, 8, 15, and 16) exhibited substantial, broad-spectrum anticancer efficacy, with IC50 values ranging from 1.58-4.27 µM relative to doxorubicin. To explore their potential modulatory capacity on receptor tyrosine kinases (RTKs), compounds 7, 8, 15, and 16 were evaluated for enzymatic efficacy against VEGFR-2, and the most active hits, 7 and 15, were further assessed against EGFR. The findings suggest a possible VEGFR/EGFR-mediated inhibition of cancer cell proliferation, with compounds 7 and 15 showing enzymatic inhibitory activity, displaying IC50 values of 0.42 and 0.23 µM for EGFR and 0.17 and 0.16 µM for VEGFR-2, respectively. Furthermore, both new hits demonstrated reduced cytotoxicity towards normal WI-38 cells, signifying favorable safety profiles. Molecular docking investigations of the active compounds within the VEGFR-2 and EGFR ATP-binding sites supported these in vitro assay results. Overall, these findings point to a potential anticancer activity and dual EGFR/VEGFR inhibitors for these compounds.

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