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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

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PubMedOncogene2026-08-30

DHCR24+ tumor epithelial cells drive cisplatin resistance in bladder cancer by enhancing cholesterol metabolism to activate lipid raft-associated MAPK signaling.

Zhao Yuanqiao Y, Xing Zhuo Z, Wang Mengmeng M, Fu Liangmin L et al.

Cisplatin-based combination therapy remains the primary treatment modality for patients with advanced bladder cancer (BCa); however, the emergence of drug resistance severely restricts clinical benefits. The molecular mechanisms underlying chemoresistance remain incompletely understood. By integrating single-cell transcriptomics with in vitro and in vivo experiments, we revealed that cholesterol metabolism was significantly hyperactivated in cisplatin-resistant BCa tissues. Further subpopulation re-clustering identified a specific chemoresistant epithelial cell subset (C3) characterized by robust cholesterol metabolism, in which the cholesterol metabolic enzyme DHCR24 was significantly upregulated and played a pivotal role in mediating cisplatin resistance in BCa. Mechanistically, the elevated expression of TFDP1 in cisplatin-resistant BCa epithelial cells upregulated DHCR24 via the formation of the TFDP1-E2F1 transcriptional complex, thereby promoting cholesterol biosynthesis. The enriched intracellular cholesterol facilitated the formation of cell membrane lipid rafts and enhanced the phosphorylation of Src, which in turn hyperactivated the downstream MAPK signaling pathway, ultimately conferring cisplatin resistance. Furthermore, the accumulated cholesterol enhanced PD-L1 protein stability, thereby impairing the efficacy of immunotherapy in BCa. Taken together, our study characterizes a specific DHCR24+ tumor epithelial subpopulation that orchestrates cisplatin resistance via the "cholesterol-lipid raft-MAPK" axis. These findings establish a clear mechanistic link between cholesterol metabolism and cisplatin sensitivity.

PMID 42668326
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PubMedMolecular therapy. Oncology2026-08-30

Additive effect of Ruta graveolens bioactive phytoconstituents and cisplatin through PKC/MEK/ERK pathway in glioblastoma.

Romano Grazia G, Morgera Valentina V, Pezone Antonio A, Messina Samantha S et al.

Glioblastoma multiforme (GBM) is a lethal malignancy with limited therapeutic options. Its aggressive progression and resistance to standard therapy necessitate the development of novel therapeutic strategies. Plant-based compounds have emerged as promising candidates for therapeutic development modulating key targets in cancer. The Ruta graveolens displays anti-inflammatory, analgesic, and antimicrobial properties. Herein, we report the anticancer potential of R. graveolens water extract (RGWE) on long-term cultures of human glioblastoma and elucidate the regulatory mechanisms driving its effect. Secondary stabilized cell cultures (U-87 MG, T98MG, and U-138 MG) and primary cell culture (FCN, MZC, and GL18-15) were either treated with RGWE and/or cis-diamminedichloroplatinum (cisplatin, CDDP). Cytostatic responses were assessed by cell viability (TB exclusion test), cell cycle (propidium iodide [PI] staining), and apoptosis (Annex-V and caspase-3) assays. We demonstrate that RGWE slows U-87 MG growth without affecting apoptosis and arrests the cell cycle in the G2/M phase. Mechanistically, RGWE interferes with PKC/MEK/ERK signaling pathway, as assessed by western blot analysis, through PKC inhibition in its active form. Furthermore, the combination of RGWE and cisplatin enables the use of a sublethal dose of the latter (0.2 μg/mL), thereby reducing cytotoxicity and the resistance to the drug. These findings reveal a novel mechanism by which RGWE controls glioblastoma growth, highlighting the therapeutic potential of targeting the PKC/MEK/ERK axis in glioma treatment.

PMID 42668569
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PubMedBiochimica et biophysica acta. Molecular basis of disease2026-08-30

EGFR and PGE2 signaling pathways mutually cooperate to promote pro-tumorigenic effects in cervical cancer.

de Azevedo Vitória R VR, Guimarães Isabella Dos S IDS, Farrapo Mario J MJ, Martins-Cardoso Karina K et al.

Cervical cancer (CC) remains a public health challenge in developing countries. Epidermal growth factor receptor (EGFR) is a receptor tyrosine kinase highly expressed in CC. Studies showed that PGE2 may transactivate EGFR in some models. However, understanding the interaction between the EGFR and PGE2 signaling pathways in CC is a key area for investigation. The Cancer Genome Atlas (TCGA) was used to evaluate gene expression correlation and clinical outcomes. Panitumumab and aspirin were employed to inhibit EGFR and COX-1/2, respectively. Cell migration was evaluated using Boyden chamber. MTT and clonogenic assays determined cell viability and clonogenicity. Western Blotting analyzed protein expression. PGE2 was measured in the supernatants of cell lines using ELISA. Flow cytometry was used for cell death assays. TCGA analysis revealed a significant positive correlation between EGFR and COX-1, COX-2, and microsomal prostaglandin E synthase-1 (mPGES-1). CC patients showed decreased overall survival upon overexpression of EGFR or COX-2. CASKI and HeLa cells were cisplatin-resistant, whereas C33A cells were chemosensitive. CASKI cells exhibited the highest EGFR levels, while HeLa cells showed highest levels of COX-2 and mPGES-1. HeLa cells showed marked upregulation of COX-2 and mPGES-1 and increased PGE2 secretion upon EGF stimulation. Moreover, PGE2 activated ERK signaling and promoted cell migration through an EGFR-dependent mechanism. Panitumumab plus aspirin impaired cell viability, clonogenicity and chemoresistance. Simultaneous stimulation with EGF and PGE2 mitigated cisplatin-induced apoptosis in CASKI cells. The interactions between EGFR and PGE2 signaling pathways link inflammation and oncogenic signaling, promoting tumor aggressive behavior.

PMID 42669370
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PubMedBiochimica et biophysica acta. Reviews on cancer2026-08-30

Systemic therapy-induced resistance and toxicity in breast cancer: Sensitization and mitigation strategies.

Samudrala Anuveda Sree AS, Nagaraju Ganji Purnachandra GP, Malla RamaRao R

Breast cancer is the most frequently reported cancer in women, with high mortality and morbidity globally. Paclitaxel, doxorubicin, tamoxifen, cisplatin, and 5-fluorouracil are cornerstones of standard-of-care treatment for primary and advanced breast cancers, targeting distinct molecular mechanisms. However, the evolution of acquired resistance primarily leads to treatment failure and progression to metastasis, ultimately to patient mortality. Furthermore, their effectiveness is limited by potential toxicities in various organs. These limitations present an extreme challenge for the management of breast cancer at the advanced stage. This review uncovers recent updates on acquired resistance mechanisms toward standard-of-care treatments driven by deeply rooted heterogeneity and aggressive nature through direct counteracting of its core action, hyperactivation of survival pathways, silencing of core cell death pathways, derepressing the expression of multidrug resistance proteins, metabolic reprogramming, epigenetic modifications, and exosome-mediated horizontal transfer of resistance phenotype. In addition, we discuss recent updates on potential strategies to overcome resistance and toxicities induced by standard-of-care treatments. Ultimately, this review helps to identify novel strategies targeting pathways to reverse resistance and reduce toxicity in breast cancer patients.

PMID 42669386
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PubMedChemistry, an Asian journal2026-08-30

Rapid Transformation of Carcinogenic 4-Nitrophenol by Nanoparticles Synthesized Using Recycled Copper Waste: A Sustainable Circular Economic Approach.

Kumar Virender V, Kumar Ravi R, Kumar Gyanendra G, Masram Dhanraj T DT et al.

Novel Cu/Cu2O-nanoparticles have been synthesized by the most economical electrochemical method utilizing metallic waste. 4-NP is a toxic pollutant affecting both animal and plant kingdom, necessitating its elimination from environment. This study demonstrates that the prepared nano-catalysts efficiently catalyse the reduction of 4-nitrophenol (4-NP) to 4-aminophenol (4-AP) at room temperature under light condition. Further, the reduction process generates amine derivatives, which are intermediates in many industrial processes. This manuscript adheres to the principles of the circular economy by generating nanoparticles through the repurposing of metallic waste discarded by both industry and domestic users. Using scrapped copper from discarded air conditioner (AC) copper tubes as electrodes, we employed an electrochemical technique to develop Cu/Cu2O nanoparticles. The synthesized nanoparticles were characterized using field emission scanning electron microscopy (FE-SEM), transmission electron (TEM), EDX spectroscopy, powder x-ray diffraction (P-XRD), Fourier transformation infrared (FTIR) spectroscopy, x-ray photoelectron spectroscopy (XPS), Raman spectroscopy, cyclic voltammetry (CV), and Brunauer-Emmett-Teller (BET) analysis. Our study confirms 99% conversion of harmful 4-NP to 4-AP in a rapid reaction time of 5 min. Synthesized nanoparticles can be reused up to four times without losing catalytic activity. UV-vis spectroscopy demonstrated that reduction follows pseudo-second-order kinetics and adsorption follows Freundlich isotherm model.

PMID 42668400
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PubMedDrug development and industrial pharmacy2026-08-30

Development of Extended-Release Oral Dosage Forms of Salbutamol Sulfate Using the Hot-Melt Extrusion Manufacturing Technique.

Ramadan Banan B, Al-Zoubi Nizar N, Migdadi Eman E, AlSuwais Alia Kh AK et al.

To fabricate and characterize extrudable polymeric matrices using a combination of ethyl cellulose (EC) and two different grades of hydroxypropyl cellulose (HPC) that can provide sustained drug release of the model drug salbutamol sulfate. Implementation of the Hot-Melt Extrusion (HME) technique in the fabrication of polymeric combinations that will provide ready-to-use matrices for sustained release dosage forms. Two formulation groups were developed; each with six formulations. The first group contained EC: HPC 370,000 ratios ranging from 55.52:13.8% to 6.9:62.46%, respectively. The second group contained EC: HPC 80,000 ranging from 59.4:10% to 9.4:60%, respectively. The release profiles were determined via in vitro studies to assess the ability of matrices to prolong salbutamol release. Solid-state characterization was also performed on the raw material and representative extrudates formulations using differential scanning calorimetry (DSC) and X-ray powder diffraction (XRPD) and polarized light microscopy (PLM). The first group formulations exhibited prolonged drug release profiles that accelerated progressively as the level of HPC 370,000 increased. In contrast, the second group formulations exhibited a noticeably faster release, demonstrating that HPC 80,000 can effectively accelerate drug release through enhanced matrix erosion and water penetration. DSC and XRPD revealed that the model drug remained in its stable crystalline state even after thermal processing via HME. PLM further confirmed drug crystallinity within the extrudates. EC-HPC matrices successfully demonstrated the feasibility of using HME to prepare sustained-release matrices for salbutamol sulfate with the ability to tune drug release by varying polymer grade and ratio.

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