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cisplatin powder (Randa / IA CALL)

✓ Approved

Nippon Kayaku Co.,Ltd. · Small Molecule · Small Molecule

What is cisplatin powder?

cisplatin powder is a small molecule developed by Nippon Kayaku Co.,Ltd.. It is approved for therapeutic indications via injectable (others) or intraarterial injection.

Drug Profile

Brand NamesRanda, IA CALL
CompanyNippon Kayaku Co.,Ltd.
Drug ClassSmall Molecule
RouteInjectable (Others), Intraarterial Injection
StatusApproved
Sources: ClinicalTrials.gov, Nippon Kayaku Co.,Ltd.

Therapeutic Indications

cisplatin powder is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Hepatic cancer✓ Approved

Related Research Articles

PubMedIndian journal of clinical biochemistry : IJCB2026-07-25

hsa-miR-3529-5p through F2RL3 Regulation as an Enhancer of Sensitivity to Cisplatin.

Moghaddam Nasibeh Sargazi NS, MohammadFakhim Baharak B, Sharifi Mohammad M, Rajabian Atefeh A et al.

The emergence of drug resistance in gastric cancer presents a critical challenge in oncological treatments, often leading to therapy failure and reduced patient survival. MicroRNAs (miRNAs) have been implicated in modulating drug resistance through various mechanisms, including altering the expression of genes involved in drug metabolism, DNA repair, and apoptosis. This study aimed to elucidate the role of miR-3529-5p in cisplatin resistance in gastric cancer by investigating its interaction with the gene F2RL3, which was identified as significantly overexpressed in cisplatin-resistant gastric cancer cells. Using RNA sequencing data and bioinformatics tools, differentially expressed genes (DEGs) were identified between cisplatin-resistant and sensitive cell lines, with F2RL3 emerging as a key gene overexpressed in resistant cells. The overexpression of miR-3529-5p using the pbud-egfb vector in AGS cells was conducted, followed by MTT assays to assess cell viability and resistance to cisplatin. qPCR was used to compare the expression of apoptosis-related genes between AGS/cis cells and AGS/miR-3529-5p/cis cells, while flow cytometry was employed to examine apoptosis levels. The results confirmed that increased miR-3529-5p expression leads to reduced F2RL3 levels, enhancing cell sensitivity to cisplatin. Cell viability assays showed a decrease in the IC50 of cisplatin in miR-3529-5p-overexpressing cells, indicating heightened drug sensitivity. Furthermore, gene expression analysis and apoptosis assays demonstrated that miR-3529-5p modulates apoptosis-related genes, promoting apoptosis in the presence of cisplatin. In conclusion, miR-3529-5p plays a significant role in reversing cisplatin resistance in gastric cancer by targeting F2RL3, suggesting its potential as a therapeutic target to enhance cisplatin efficacy in gastric cancer treatment.

PMID 42500345
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PubMedIn vitro cellular & developmental biology. Animal2026-07-25

Daphnetin alleviates cisplatin-induced acute kidney injury by inhibiting the HIF-1α signaling pathway.

Wan Li L, Lu Congxian C, Xue Chunju C, Deng Xiaofeng X

Cisplatin-induced acute kidney injury (AKI) limits its clinical use, and effective renoprotective agents are lacking. Daphnetin (DAP), a natural coumarin, exhibits anti-inflammatory and antioxidant properties, but its role and mechanism in cisplatin nephrotoxicity remain unclear. This study investigates whether DAP protects against cisplatin-induced renal tubular injury and elucidates the involvement of the HIF-1α signaling pathway. A rat model of cisplatin-induced AKI and an in vitro HK-2 cell injury model were used. Renal function, histopathology, injury markers (KIM-1, NGAL), inflammatory cytokines (TNF-α, IL-1β, IL-6, TGF-β), cell viability, proliferation, apoptosis, and HIF-1α expression were assessed. Bioinformatics analysis and rescue experiments using the HIF-1α activator ML228 were performed. DAP significantly ameliorated cisplatin-induced renal dysfunction, pathological damage, and inflammatory responses in rats. In HK-2 cells, DAP enhanced viability and proliferation, reduced apoptosis, and downregulated KIM-1, NGAL, and pro-inflammatory cytokines. HIF-1α protein and mRNA level was upregulated by cisplatin, and DAP reversed this effect. Bioinformatics and KEGG analysis identified the HIF-1 pathway as the most enriched. Activation of HIF-1α by ML228 abolished DAP's protective effects, confirming the pathway's critical role. DAP alleviates cisplatin-induced AKI by inhibiting the HIF-1α signaling pathway. This natural compound represents a promising candidate for preventing chemotherapy-related renal injury.

PMID 42498919
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PubMedSmart molecules : open access2026-07-25

Redox-responsive dual-drug nanomedicine integrating cisplatin and trypsin for synergistic reversal of tumor chemoresistance.

Yin Xiaolan X, Wang Qi Q, Zhang Ming M, Zhang Cheng C et al.

To overcome cisplatin resistance without increasing systemic toxicity, we rationally elaborated a glutathione-activatable prodrug nanomedicine that chemically co-encapsulates cisplatin and a masked protease. First, a redox-labile succinimide linker (NC-ss-COOH) was covalently grafted onto the ε-amino groups of trypsin to create a "pro-protease" (ssTrypsin) whose catalytic activity is completely silenced in circulation but instantly restored (≥96%) upon cleavage by intratumoral GSH. Simultaneously, cisplatin was stably coordinated to the carboxyl-rich backbone of cRGD-PEG-polyglutamic acid and carboxyl-rich ssTrypsin, forming a polymer-Pt(II) prodrug that prevents premature Pt-GSH adduct formation. These two prodrugs co-self-assemble into potent anti-tumor nanoconstructs that actively target αvβ3/αvβ5-overexpressing tumors. Upon GSH-triggered activation, the dual-drug combination exerts complementary actions: (i) released cisplatin directly damages DNA, while (ii) reactivated trypsin proteolytically degrades all intracellular, cytomembrane, and extracellular proteins as possible (including DNA-repair proteins), collectively re-sensitizing resistant cells. This "prodrug + pro-enzyme" strategy yields a 2.5-fold reduction in IC50 against A2780DDP cells and 77% tumor suppression in vivo, all with minimal off-target toxicity.

PMID 42500704
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PubMedJournal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS)2026-07-25

Cisplatin-induced inflammatory liver injury via promoting free radicals' accumulation and Bax/Caspase-3 apoptotic signaling cascades: A possible mitigating role of high-purity selenium.

Aboraya Dina M DM, Risha Engy F EF, El Baz Ayman A, Rajab Bodour S BS et al.

Cisplatin is a prevalent anti-tumor agent despite its association with DNA damage, oxidative stress, myelosuppression, and hepatotoxicity, which may limit its use. The current study aims to assess the mitigating effect of selenium on cisplatin-induced hepatotoxicity. Thirty-two adult albino rats were evenly divided into four groups: the control group received normal saline, the CIS group was IP injected with a single dose of cisplatin (7.5 mg/kg BW) on the 22nd day, the SE group received selenium (1 mg/kg BW, orally) for 21 days, and the SE + CIS group received selenium daily followed by a single IP dose of cisplatin. Samples were collected for hemogram, liver function tests, hepatic redox status, expression of pro- and anti-inflammatory cytokines, and evaluation of pro-apoptotic proteins. In the CIS group, hepatobiliary enzymes, bilirubin, cholesterol, triglycerides, blood glucose, hepatic MDA, and TNF-α mRNA expression increased significantly (P ≤ 0.001) and correlated positively (r = 0.99-0.80) with hepatocyte necrosis, pro-apoptotic Bax, and Caspase-3 markers immunoreactivity. Total protein, albumin, globulin, SOD, CAT, GSH, and IL-10 expression significantly decreased (P ≤ 0.001) and correlated negatively (r = -0.99 to -0.80) with hepatopathies and pro-apoptotic marker expression. Indeed, hepatic damage scores and immunoreactivity for the pro-apoptotic markers Bax and caspase-3 were significantly ameliorated in the SE + CIS group. These mitigations showed strong correlations with improved liver function panel results, antioxidant capacity, and hepatocyte expression of IL-10 and TNF-α. Pretreatment with selenium mitigates cisplatin-induced hepatocellular toxicity by promoting IL-10 expression, quenching free radicals, and activating downstream Bax/Caspase-3 apoptotic signaling cascades.

PMID 42497513
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PubMedTurkish journal of medical sciences2026-07-25

In silico evaluation of the role of PEA3 subfamily ETS transcription factors in chemoresistance in ovarian cancer.

Sökmen Fevzi Coşkun FC, Kardana Laika L, Yilmaz Hikmet H, Özketen Ahmet Çağlar AÇ et al.

The E26 transformation-specific family of transcription factors regulates the cell cycle and apoptosis that are crucial for carcinogenesis. More specifically, the PEA3 subfamily-comprising ETS variant (ETV) transcription factors ETV1, ETV4, and ETV5-has been implicated in multiple oncogenic signaling pathways and chemotherapy resistance. While cisplatin is still a widely used chemotherapeutic treatment for ovarian cancer, its therapeutic efficacy is sometimes limited by the induction of resistance mechanisms. The present study investigates the potential role of PEA3 subfamily genes in cisplatin resistance in ovarian cancer through comprehensive in silico analyses. Cisplatin response data for ovarian cancer were obtained from the Cancer Treatment Response Database version 2 (CTR-DB2), and the relevant dataset was analyzed. Candidate genes, including members of the PEA3 transcription factor subfamily, were analyzed with a multigene biomarker model, and a receiver operating characteristic analysis was used to measure predictive ability. GEPIA2, KMplotter, and cBioPortal were used for survival analysis, while the TNMplot, cBioPortal, and Clinical Proteomic Tumor Analysis Consortium datasets were used for multiomics characterization and differential expression. The ETV4-CIC gene pair in the CTR-DB2 validation dataset achieved the highest predictive performance for cisplatin response in ovarian cancer with an area-under-curve of 0.939, clearly separating responders from nonresponders. No other gene combinations outperformed this model, demonstrating only moderate predictive capacity. The ETV4-CIC gene pair was also associated with disease-free survival. Differential expression analysis showed downregulation of CIC and upregulation of ETV4 in tumor tissues. Genomic and proteomic analyses confirmed alterations in both genes, while correlation analysis suggested complementary biological roles. The ETV4-CIC gene pair effectively discriminated between cisplatin responders and nonresponders in ovarian cancer. Accordingly, the ETV4-CIC signature may serve as a useful biomarker for cisplatin response prediction and patient stratification in precision oncology.

PMID 42499433
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PubMedEuropean journal of oncology nursing : the official journal of European Oncology Nursing Society2026-07-25

Exploring the usability of a point-of-care hearing screening by oncology registered nurses with adult cancer patients during Cisplatin chemotherapy - A convergent mixed methods study.

Rooker Jennessa J, Marshall Victoria K VK, Johnson Ayesha A, Sanchez Victoria V et al.

Ototoxicity, defined as hearing loss and tinnitus, affects more than 50% of cancer survivors treated with Cisplatin chemotherapy. Despite national recommendations for routine symptom monitoring, hearing screenings remain underutilized in oncology. Point-of-care (POC) technologies offer a promising solution to enhance ototoxicity detection during chemotherapy. This study aimed to explore the usability of an iPad-based POC auditory screening system administered by oncology nurses in ambulatory infusion settings. A convergent mixed-methods study was conducted. Participants included adult patients undergoing Cisplatin chemotherapy treatment, and infusion nurses who were trained to use the SHOEBOX Ltd. iPad-based audiometry application. Quantitative usability data were collected with the System Usability Scale (SUS), while qualitative data were obtained through semi-structured interviews with eight patients and five nurses. Thematic analysis was used to code transcripts, with integration of results achieved through methodological triangulation. The average SUS score among patients (n = 5) was 84.5 (SD = 29.4), and among nurses (n = 5) was 92 (SD = 7.6), indicating high system usability. Qualitative findings supported these results, with most patients describing the hearing screen as "easy" and even gave them something to do during chemotherapy. Reported barriers included environmental noise and patient complications related to treatment. Nurses found the screening system easy to implement and reported increased awareness of ototoxicity symptoms during chemotherapy. POC auditory screening tools may enhance ototoxicity monitoring in cancer care by supporting early symptom recognition, fostering timely clinical response, and increasing patient and nurse engagement.

PMID 42497611
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