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cisplatin powder (Randa / IA CALL)

✓ Approved

Nippon Kayaku Co.,Ltd. · 小分子 · 小分子

什么是 cisplatin powder？

cisplatin powder 是一种小分子，由Nippon Kayaku Co.,Ltd.研发。该药已获批，用于治疗相关适应症，给药途径：Injectable (Others)、Intraarterial Injection。

药物档案

商品名Randa, IA CALL
公司Nippon Kayaku Co.,Ltd.
药物类别小分子
给药途径Injectable (Others), Intraarterial Injection
状态Approved
来源： ClinicalTrials.gov, Nippon Kayaku Co.,Ltd.

治疗适应症

cisplatin powder 针对 1 个适应症，涉及 1 个治疗领域。

治疗领域疾病/病症分期
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Hepatic cancer✓ Approved

相关研究文献

PubMedInternational journal of molecular sciences2026-10-27

Modulation of FOXO3 Transcriptional Regulation by Cisplatin and Curcumin in Human Embryonic Kidney Cells.

Coronado-Moreno Edson E, Mendoza-Santos Victor V, Larre Isabel I, González-Cázares Diana D et al.

Cisplatin is a highly effective anti-neoplastic agent, but its clinical application is limited by its association with severe nephrotoxicity. Although extensive research has identified several mechanisms underlying cisplatin-induced nephrotoxicity, the precise molecular pathways remain incompletely understood. Recent studies have highlighted the role of intrinsic survival, senescence, and longevity signaling pathways, including those governed by the FOXO3 transcription factor. In this study, we examined the effects of cisplatin and curcumin on the DNA methylation status and mRNA expression of FOXO3 in human embryonic kidney (HEK293) cells. Our results indicate that the FOXO3 promoter is methylated in cisplatin-treated cells, and that cisplatin regulates FOXO3 transcription in a dose-dependent manner. Quantitative RT-qPCR revealed that moderate cytotoxic concentrations of cisplatin (10 and 40 µM) significantly downregulate FOXO3 mRNA. Furthermore, co-treatment with the antioxidant curcumin successfully restored and enhanced FOXO3 expression at moderate cisplatin doses (10 µM) but failed to rescue expression at high doses (40 µM). Moreover, curcumin treatment (10 µM) reverses the effects of low-dose, but not high-dose, cisplatin (40 and 60 µM). Taken together, these findings provide a foundation for understanding the epigenetic and transcriptional regulation of FOXO3 and highlight its potential as a target for antioxidant-mediated nephroprotection and its role in cell survival.

PMID 42941746
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PubMedLife (Basel, Switzerland)2026-10-27

The Pharmacogenomics of Cisplatin-Induced Ototoxicity.

Harman David D, Lim Chiao Xin CX, Kichenadasse Ganessan G, Morrison Janna J et al.

Cisplatin is a first line treatment for a wide range of cancers; one commonly observed adverse drug reaction (ADR) of cisplatin is ototoxicity. Onset of ototoxicity from cisplatin is inconsistent and no single risk factor can reliably predict whether a patient will develop ototoxicity. A genetic factor has been explored for these reasons. This study reviews and summarizes the strongest evidence toward a genetic association. A search of the literature was conducted across three databases for studies exploring the genetic association with cisplatin ototoxicity. 15 unique genes were observed by at least two unique studies with single nucleotide polymorphisms (SNPs), which significantly affected the likelihood of cisplatin-induced ototoxicity. There are many SNPs across a variety of genes that can significantly affect the likelihood of cisplatin-induced ototoxicity. Comparing the findings of studies is difficult because of significant heterogeneity in patient characteristics, treatment plans, and the classification of ototoxicity. Despite this, variants in ACYP2 (rs1872328), SLC22A2 (rs316019), and TLR4 (rs10759932) emerged as the most reproducible findings in this review.

PMID 42942184
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PubMedBiomedicines2026-10-27

A Non-Linear Ototoxic Response to Cisplatin Is Associated with Autophagy and PTEN/PI3K/AKT Signaling in Cochlear Hair Cells and Spiral Ganglion Neurons.

Li Yingru Y, Han Miaomiao M, Lu Cheng C, Tang Jingyi J et al.

Background: Cisplatin-induced ototoxicity is generally considered dose-dependent. However, cellular adaptive responses under severe cisplatin stress remain incompletely understood. This study aimed to investigate the non-linear ototoxic response to cisplatin and explore the potential involvement of autophagy in the survival of cochlear hair cells and spiral ganglion neurons. Methods: Cochlear explants from postnatal day 3 rats and HEI-OC1 cells were treated with different concentrations of cisplatin (0-400 μM). HCs and SGNs injury and apoptosis were assessed by immunofluorescence staining, hair cell counting, TUNEL assays, cell viability assays, and Western blotting. PCR arrays were used to characterize neurotransmission- and autophagy-related gene expression, and transmission electron microscopy was performed to examine autophagic structures. Western blotting was further used to evaluate autophagy-related proteins and PTEN/PI3K/AKT signaling. Results: Cisplatin induced a non-linear ototoxic response in cochlear explants. Hair cell loss increased from approximately 70% at 10 μM to over 90% at 100 μM, but was markedly reduced at 400 μM. This reduced injury was accompanied by decreased apoptosis, increased LC3-II, decreased P62, and altered PTEN/PI3K/AKT signaling. In contrast, HEI-OC1 cells showed progressively reduced viability with increasing cisplatin concentration, suggesting a model-dependent response. Conclusions: High-concentration cisplatin was associated with reduced cochlear injury and enhanced autophagy-related activity in cochlear explants. These findings suggest that autophagy and PTEN/PI3K/AKT signaling are associated with the non-linear response to severe cisplatin stress.

PMID 42940183
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PubMedBiology2026-10-27

ARMCX3 Regulates Breast Cancer Progression and Cisplatin Responsiveness Through p53-Related Signaling.

Deng Xinyan X, Ma Haixiang H, Zhang Jiajie J, Huang Xiyang X et al.

Despite substantial advances in diagnosis and treatment, breast malignancy continues to cause considerable morbidity and mortality. Cisplatin has demonstrated therapeutic activity in selected patients with advanced breast cancer, but its clinical use may be limited by treatment resistance. Although ARMCX3 is implicated in other cancers, its role and underlying mechanisms in breast cancer remain unclear. We investigated ARMCX3 functions using depletion and rescue experiments, and ARMCX3 depletion reduced cell growth, migration, and invasion and increased cisplatin sensitivity in vitro, while re-expression rescued these phenotypes. Transcriptomic analysis revealed enrichment of the p53 pathway following ARMCX3 depletion. PFT-α treatment suppressed the protein level of p53 and attenuated the effects of ARMCX3 knockdown on cell proliferation, migration, invasion, cell-cycle arrest, and cisplatin response. ARMCX3 knockdown was also associated with altered DNA damage response signaling, enhanced cisplatin-induced apoptosis and suppressed tumor growth in vivo, and all these effects were attenuated by PFT-α treatment. These findings suggest that p53-associated signaling contributes to the effects of ARMCX3 depletion on breast cancer progression and cisplatin responsiveness. These results may help inform future studies exploring ARMCX3-associated signaling in the context of cisplatin response.

PMID 42939454
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PubMedMaterials (Basel, Switzerland)2026-10-27

Local Mo6+ Coordination and Textural Accessibility, Rather than Bulk Phase, Correlate with the Peroxidase-Mimetic Reactivity of CoMoO4 Nanopowders.

Rosić Milena M, Mojović Zorica Z, Pagnacco Maja C MC, Senćanski Jelena V JV et al.

Whether the bulk crystallographic phase determines the H2O2 reactivity of oxide nanopowders has direct implications for catalyst design. Three glycine-nitrate-derived CoMoO4 nanopowders-as-synthesized, calcined at 450 °C (both β-CoMoO4 by XRD), and calcined at 1000 °C (α-CoMoO4)-were studied by ATR-FTIR spectroscopy, the Briggs-Rauscher (BR) oscillatory reaction, cyclic voltammetry (CV), and electrochemical impedance spectroscopy. Deconvolution of the Mo-O stretching region with a uniform Voigt line shape resolves octahedral (α-type) and tetrahedral (β-type) Mo6+ components in both β-classified powders, indicating short-range coordination heterogeneity not detected by XRD. In the BR reaction (n = 3), the 450 °C powder suppresses oscillations at ≤0.002 g, whereas the as-synthesized powder still oscillates at 0.040 g (slope of the τosc decrease is 5172 ± 406 s g-1), and the bulk-α 1000 °C powder is about four times less active per gram than the as-synthesized powder. CV supports the highest activity of the 450 °C powder. A semi-quantitative descriptor, Φ = ρα × SBET, combining the FTIR α-type band-area fraction with the BET surface area, identifies the most active powder but does not discriminate between the two less active ones. Within this series, bulk phase identity alone does not predict peroxidase-mimetic activity.

PMID 42941058
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PubMedInternational journal of molecular sciences2026-10-27

Bioactive and Molecular Characterization of Mealworm (Tenebrio molitor) Powder: Nutritional and Functional Implications for Crackers.

Zielińska Ewelina E, Jakubczyk Anna A, Jaglińska Kamila K, Polak Beata B

Edible insects are increasingly recognized as a viable alternative food source, highlighting the urgent need for systematic research into their integration into conventional food products. This study examined the effect of adding mealworm powder (Tenebrio molitor) to crackers, focusing on factors such as color, texture, nutritional value, antioxidant properties, starch digestibility, and molecular structure. As the level of mealworm powder increased (from 2% to 10%), the crackers became darker, while instrumental hardness and fracture time decreased, indicating that a more brittle structure formed. Nutritionally, the enriched crackers contained higher protein, fat, and mineral content, while their carbohydrate content decreased; moreover, their protein profile was modified. Antioxidant activity and total phenolic content also rose in proportion to the level of mealworm enrichment. FTIR analysis revealed differences in spectral regions associated with proteins, lipids, and carbohydrates, indicating compositional and local molecular-environment changes following mealworm powder incorporation. Mealworm powder incorporation markedly decreased rapidly digestible starch and increased slowly digestible starch, whereas the predicted glycemic index showed only a modest but statistically significant reduction at higher supplementation levels. Furthermore, sensory evaluation indicated that consumer acceptance was optimal at a low inclusion level of 2%. Overall, mealworm powder represents a promising ingredient for improving selected nutritional and functional characteristics of crackers; however, its inclusion level should be optimized to maintain sensory quality.

PMID 42942143
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