doxorubicin hydrochloride

In this study, doxorubicin (DOX) and PD-L1 siRNA were initially loaded into ZIF-8 to synthesize highly stable nanocomplex RNA-DOX@ZIF-8 (RDZ)...Furthermore, in a murine osteosarcoma recurrence model, Gel@RDZ exhibited optimal immune cell infiltration, substantially reduced tumor recurrence, and markedly enhanced the tumor-killing efficacy of CD8+ T cells. Therefore, the development of a multifunctional hydrogel system (Gel@RDZ) provides a comprehensive treatment for postoperative maxillofacial osteosarcoma.

In an in-vivo solid Ehrlich carcinoma (SEC) mouse model, compound 6b significantly reduced tumor weight and volume, exceeding the efficacy of doxorubicin...Computational analyses, including molecular docking, molecular dynamics simulations, and DFT calculations, provided insights into the binding stability and interaction mechanisms of 6b with CDK2 and PIM1, while in-silico pharmacokinetic and toxicity evaluations confirmed its favorable drug-like profile and safety. This study highlights compound 6b as a promising dual CDK2/PIM1 inhibitor with potent anti-cancer activity and selectivity, paving the way for its further optimization and development as a lead molecule in cancer therapy.

Compared to NK-exos, NK-exos-Dox enhanced cytotoxicity and apoptosis in Hep3B cells by upregulating pro-apoptotic proteins (Bax, cytochrome c, cleaved caspase 3, and cleaved PARP) and inhibiting the anti-apoptotic protein (Bcl-2). These findings suggest that NK-exos-Dox significantly boost anti-tumor effects by activating specific cytotoxic molecules, offering promising therapeutic opportunities for solid tumor treatment, including HCC.

That is why in case of small tumours (<200mL), patients can be treated with less intensive protocols, as Saint Jude's (low-dose semi-continuous cyclophosphamide/doxorubicin regimen as induction chemotherapy and vincristine/actinomycin courses as maintenance therapy), setting aside the option of classical VDC/IE protocol for larger tumors. Local treatment must rely on carcinologic surgery, with the aim to avoid radiotherapy when possible. Patients with metastatic disease have bad prognosis resemble classical Ewing sarcoma, and have to be treated accordingly.

In conclusion, combination of parthenolide and doxorubicin exert enhanced cytotoxic effects via increased apoptosis and modulation of miR-27b and the MET signaling pathway in Raji cells, regulatory relationship between miR-27b and the MET signaling pathway may contribute to the observed therapeutic benefits. Further research is required to clarify the molecular mechanisms and therapeutic applications of this combination strategy.

These strategies include BRD and extraterminal (BET) inhibitors, trabectedin, inhibitors of the EP300 histone acetyltransferase, and histone deacetylase inhibitors such as vorinostat. In the absence of clinical trials, the results from this review suggest that trabectedin-based or ifosfamide-based regimens, particularly in combination with doxorubicin, may offer a reasonable approach as frontline therapy for NUT sarcomas.

In Sim cotreated cells increased Doxorubicin uptake and enhanced Doxorubicin-induced cytotoxic effects have been demonstrated together with reduced migratory capacity. Our data support the notion that Sim cotreatment could be a possible strategy to overcome chemoresistance, since the observed increase in Cx43 membrane levels, and the concomitant reduction of Cx43 phosphorylation, could be responsible for increased sensitization of cells to Doxorubicin treatment.

P1/2, N=22, Enrolling by invitation, St. Petersburg State Pavlov Medical University

P2, N=112, Active, not recruiting, Dana-Farber Cancer Institute | Trial completion date: Dec 2024 --> Mar 2025

The objective of the study was to determine the efficacy of secukinumab (SEC), a completely human monoclonal IgG1/κ antibody that targets IL-17A, in ameliorating DOX-induced cardiotoxicity (DIC). Furthermore, it mitigated the heightened activation of the NF-κB/NLRP3 pathway caused by DOX. This study shows that IL-17A neutralization can prevent DIC by regulating the NF-κB/NLRP3/Caspase-1/IL-1β pathway to be used as potential therapeutic target for CVDs.

This catalytic SNA nanocarrier, built on a DNA core-shell framework, combines the ribozyme with doxorubicin (Dox) to form the ApRz-CS/Dox nanoplatform...Within the target cells, the ribozyme is released in response to overexpressed miR-21, facilitating the cleavage of polo-like kinase 1 mRNA. This integrated approach effectively combines gene therapy with the chemotherapeutic effects of Dox, addressing the challenges associated with the delivery of newly developed nucleic acid drugs and offering a promising strategy for enhanced cancer treatment.

Cellular senescence was induced using doxorubicin, a DNA-damaging agent...Our hiPSC-derived lung cell senescent model reproduces key aspects of human lung senescence and offer an in vitro tool for studying age-related lung disease mechanisms and therapeutic interventions. This model has potential applications in exploring the impact of environmental factors (e.g., toxins, infectious pathogens, etc.) on the senescent lung and assessing treatments that could mitigate pathologies associated with pulmonary aging including barrier impairment, inflammation and fibrosis.

DIG-mediated HIF-1α inhibition enhanced TNBC sensitivity to DOX, leading to significant suppression of both primary tumor growth and pulmonary metastasis. This study presents a promising and clinically feasible strategy for TNBC and other hypoxia-driven malignancies.

Olmesartan may represent a promising therapy for DOX-elicited testicular dysfunction, possibly via dose-dependent antioxidant, anti-pyroptotic, anti-inflammatory, and autophagy enhancing effects.

P2, N=153, Active, not recruiting, St. Jude Children's Research Hospital | Trial completion date: Dec 2024 --> Dec 2025

Furthermore, Sirius-red staining of cardiac sections showed higher fibrosis levels (p < 0.0001) in Dox-STZ compared to Dox or STZ alone. All together, these results demonstrate that STZ precipitates and unmask cardiac dysfunction in previously treated Dox animals.

Importantly, the impact of SA treatment against DOX-promoted cardiac deterioration is by targeting the Nrf-2/Keap-1/HO-1/NQO-1 signaling pathway, which in turn induces the antioxidant agents. These findings suggest that SA treatment could potentially mitigate cardiac toxicity during DOX-based chemotherapy.

Our study underscores the unique epidemiological profile of peripheral T-cell lymphoma in Latin America, with a high prevalence of adult T-cell leukaemia or lymphoma and extranodal natural killer T-cell lymphoma. These findings present a crucial opportunity to prioritise clinical trials on these rare subtypes of peripheral T-cell lymphoma by integrating Latin American countries into global research. However, our findings require further validation in robust epidemiological studies.

In vivo, treatment with LC3siRNA-NPs and DOX in a TNBC xenograft model resulted in superior tumor growth suppression compared to that with monotherapy alone. Our findings highlight the potential of autophagy-targeting nanocarriers to improve chemotherapy outcomes and provide an effective approach to TNBC treatment by enhancing chemotherapeutic sensitivity and reducing tumor resistance.

Preclinical studies have also suggested potential synergy with doxorubicin and eribulin, although these findings have yet to be validated in randomised clinical trials. Ongoing studies, such as the SeliSarc trial (NCT04595994) evaluating selinexor in combination with gemcitabine and the NRSTS2021 trial (NCT06239272) evaluating selinexor in paediatric soft tissue sarcoma, aim to further define its role. The results of these studies will be critical in determining whether selinexor can be incorporated into standard sarcoma treatment.

Single-agent ICI therapy, such as cemiplimab (ORR 27.8%), has shown responses primarily in UV- and radiation-associated angiosarcomas, likely due to their higher tumor mutation burden (TMB), while dual ICI therapy (SWOG S1609, ORR 25%) suggests potential benefit but remains limited in cutaneous disease...The Alliance A091902 first-line trial (paclitaxel ± nivolumab) found no overall PFS benefit, though scalp/face angiosarcoma patients appeared to fare better, raising the question of whether ICI alone might be equally effective in this subset. The South Korean paclitaxel + avelumab trial (ORR 50%) showed promising response rates, but the lack of detailed subgroup analysis limits interpretation. Other chemotherapy-ICI combinations, such as doxorubicin plus pembrolizumab, have shown isolated responses but require further study in larger cohorts. Moving forward, better biomarkers are critical for identifying which patients benefit most from ICIs, and while TKI-ICI combinations appear to hold the most promise, chemotherapy-ICI strategies need further refinement to optimize sequencing and patient selection in angiosarcoma treatment.

The outcomes from in vitro assays corroborated with the molecular docking results and hence, on authenticating the potentiality of AAE's anti-neoplastic effect via. in vivo models, pre-clinical and clinical trials, Allium ascalonicum can be articulated to a prospective anti-neoplastic drug for treating TNBC.

Replicative, mitotic, oxidative, and genotoxic forms of TIS were induced in p16-null/p53-proficient, BAX-deficient, and BRCA1-mutant cancer cells using mechanistically distinct TIS-inducing cancer therapeutics, including palbociclib, alisertib, doxorubicin, bleomycin, and olaparib...Furthermore, regardless of senescence-inducing therapeutic, stable/transient senescence acquisition, or genetic context, all TIS phenotypes shared a variable but significant senolytic response to the BCL-xL-selective BH3 mimetic A1331852. These findings may help to rethink the traditional assumption of the primed apoptotic landscape of TIS cancer cells. BCL-xL is a conserved anti-apoptotic effector of the TIS BCL2/BH3 interactome that can be exploited to maximize the efficacy of "one-two punch" senogenic-senolytic strategies.

Loss of ANGEL2 in cancer cell lines resulted in increased 2D and 3D spheroid cell growth, and resistance to doxorubicin and etoposide. Together, we conclude that ANGEL2 modulates the EIF4E-RBM38 complex to enhance wildtype TP53 translation, and further, the Pep7 peptide may be explored as a therapeutic strategy for cancers which harbor wildtype TP53 expression. Implications: Loss of ANGEL2 contributes to decreased wildtype TP53 translation promoting doxorubicin resistance which can be rescued via an ANGEL2-derived peptide.

PMDDH markedly reduces Dox-induced cardiotoxicity by preserving mitochondrial function, reducing reactive oxygen species (ROS) production, and inducing protective autophagy in cardiomyocytes. These findings position PMDDH as a promising dual-function nanomedicine that enhances the anti-tumor efficacy of Dox while minimizing its systemic toxicity, offering a safer and more effective alternative for cancer therapy.

Adjuvant chemotherapy included 4 cycles of doxorubicin hydrochloride (Adriamycin) and cyclophosphamide followed by 4 cycles of docetaxel (Taxotere). Optimal treatment of AcCC is the same as that for invasive breast cancer. The prognosis is generally good, with adjuvant therapy after surgery.

P1/2, N=304, Recruiting, Genmab | N=184 --> 304

P3, N=177, Active, not recruiting, University of Arkansas | Trial completion date: Aug 2025 --> Aug 2026 | Trial primary completion date: Aug 2025 --> Aug 2026

Blocking PD-L1 and LAG-3 in combination with doxorubicin is therapeutic potential approach for breast cancer and offers hope for improved patient outcomes.

Silymarin may enhance anti-tumor effects of doxorubicin through modulating autophagy, angiogenesis, and apoptosis, in-vitro.

P2/3, N=401, Active, not recruiting, Boehringer Ingelheim | Trial completion date: May 2026 --> Nov 2025

Our findings indicate that CDC20 safeguards the heart against DOX-induced cardiotoxicity by modulating CCDC69 degradation without compromising the antitumor efficacy of DOX.

P2, N=70, Not yet recruiting, University of California, San Francisco

A doxorubicin (DOX) and dual-gene plasmid (MAC pDNA, encoding both MHC-I/ASMTNMELM and CD55-shRNA) coloaded drug delivery system (LCPN@ACD) with tumor targeting and charge/size dual-conversion properties was prepared...LCPN@ACD downregulated tumor cell CD55 expression, increased the proportion of ICOSL+ B cells and CTLs, and reversed the TIME, thus greatly improving the efficacy of αPD-1 and CAR-T therapies. The application of this in situ tumor cell engineering strategy eliminated the source of tumor immune escape, providing new ideas for solving the challenges of clinical immunotherapy.

P3, N=623, Completed, The Lymphoma Academic Research Organisation | Active, not recruiting --> Completed | Trial completion date: Aug 2025 --> Jan 2025

Drug sensitivity analysis indicated CS2's higher sensitivity to cisplatin, doxorubicin, paclitaxel, and sunitinib, whereas CS1 was more sensitive to bicalutamide and FH535. Twenty-four paired tumors and adjacent normal tissues by immunohistochemical staining further demonstrated the prognostic value of CXCL17. In conclusion, we identified two distinct molecular subtypes of TC with significant implications for prognosis, genetic alterations, pathway activation, and treatment response.

Our study suggested that TZP attenuated oxidative stress and cardiomyocyte apoptosis by modulating HRD1-mediated Nrf2 expression and activity, thereby protecting against the cardiotoxic effects exerted by DOX. These results supported that TZP might be a promising therapeutic option for reducing chemotherapy-related cardiotoxicity.

Thus, the disruption of mitochondrial remodeling and impaired protein ubiquitination emerge as enduring consequences of DOX-induced cardiotoxicity, persisting for even 2 months after DOX exposure. This underscores the long-lasting impact of DOX, with significant effects continuing beyond the period of administration, which advocates for longer clinical surveillance.

P=N/A, N=200, Completed, Federico II University

Bioinformatics analyses and enrichment analyses of RNA-seq data revealed activation of Pi3K pathway which is further validated in-vitro. These results provide evidence of the unexpected pro-angiogenic response of SH-SY5Y cells to doxorubicin treatment and suggest the potential use of multi-modal therapeutic regimens for a more comprehensive approach to NB treatment.

We report here that the cooperative binding of doxorubicin (Dox) with actinomycin D (ActD) enhances the specificity for consecutive GCCG sites in DNA. In vivo, the combination significantly suppresses tumor growth and outperforms the standard Dox and cyclophosphamide regimen in inhibiting metastasis. This study highlights targeting the activated EGFR pathway with sequence-specific DNA-targeting drug combinations as a potential TNBC treatment.

DHA combined with DOX produces significantly enhanced effects for inhibiting cell proliferation and inducing apoptosis in MDA-MB-231 cells possibly as result of DHA-mediated negative regulation of the STAT3/HIF-1α pathway.