Delving into the Latest Updates on Sepantronium Bromide with Synapse

Background:
Carboplatin-paclitaxel is a commonly used chemotherapy combination for advanced non-small-cell lung carcinoma (NSCLC) and other solid tumors. In a randomized clinical trial, the combination of carboplatin, paclitaxel, and the additional chemotherapy drug bevacizumab had a better response rate and survival compared to carboplatin and paclitaxel alone. However, this trial treated only patients with a specific diagnosis and treatment risks. Further research is needed to determine whether this combination is useful for other diagnoses.
YM155 is a drug that targets a type of chemical often found in cancer cells. It has been investigated in several phase I and phase II clinical trials, and it has been shown to be well tolerated and moderately effective in treating advanced NSCLC in patients who had not responded well to one or two standard treatments.
Objectives:
- To determine the efficacy of the combination of carboplatin, paclitaxel, and YM155 in the treatment of non-small-cell lung cancer.
Eligibility:
- Individuals 18 years of age and older who have been diagnosed with advanced non-small-cell lung carcinoma or other solid tumors for which standard therapy is not likely to be effective.
Design:
Before the start of the study, participants will be screened with a medical history, blood tests, imaging scans of the affected areas, tumor biopsies, and other tests as directed by the study doctors.
Participants will be treated for six 21-day cycles, or 18 weeks of treatment. Each cycle will include blood tests and imaging studies as required.
On day 1 of each cycle, participants will receive an infusion of paclitaxel and carboplatin, followed by a 4-day infusion of YM155 (through a portable electronic infusion pump).
Participants will have a computed tomography scan or other imaging every other cycle (approximately every 6 weeks) to determine whether the therapy is affecting the cancer site.
After the sixth cycle, participants will return for follow-up visits at least every 3 months, and will be asked to remain in contact with the researchers to allow further study of the long-term effects of the treatment.

Start Date01 Feb 2010

Sponsor / Collaborator

National Cancer Institute

NCT01038804

/ CompletedPhase 2

A Phase II, Multicenter, Open-Label, Randomized Study of YM155 Plus Docetaxel as First-Line Treatment in Subjects With HER2 Negative Metastatic Breast Cancer

The purpose of this study is to evaluate survival, response rate, safety and tolerability of YM155 given in combination with docetaxel as first-line treatment in subjects with human epidermal growth factor 2 non-overexpressing (HER2 negative) metastatic breast cancer.

Start Date01 Dec 2009

Sponsor / Collaborator

Astellas Pharma, Inc.

100 Clinical Results associated with Sepantronium Bromide

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100 Translational Medicine associated with Sepantronium Bromide

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100 Patents (Medical) associated with Sepantronium Bromide

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543

Literatures (Medical) associated with Sepantronium Bromide

01 Jun 2025·Vascular Pharmacology

Survivin in cardiovascular diseases and its therapeutic potential

Review

Author: Inserra, Gabrielle ; Gupte, Sachin ; Babatunde, Sefunmi ; Krug, Alanna ; Pham, Khanh ; Brazzo, Joseph A ; Drewes, Rhonda ; Mousso, Thomas ; Jong, Jessica ; Bae, Yongho ; Biber, John

Aberrant changes in cell behaviors, such as proliferation, apoptosis, and migration, are some of the contributing factors to the development of various cardiovascular diseases (CVDs) and pathologies, including atherosclerosis, neointimal hyperplasia, and heart failure. In recent years, numerous studies have identified survivin, a key player in the anti-apoptotic pathway, to be extensively involved in modulating cellular functioning in cancer, with many reaching clinical trials. Though seemingly different, CVDs and cancer share abundant similarities regarding abnormal cell modifications and behaviors. This overlap has sparked growing interest in investigating survivin as a therapeutic target in the context of CVD. With new findings emerging rapidly, a comprehensive understanding of survivin's role in cardiovascular pathology is crucial to revealing its full therapeutic potential and translating these discoveries into effective treatments. This review discusses recent findings of survivin in CVDs and related pathologies, focusing on its dual role in promoting proliferation and inhibiting apoptosis, specifically in atherosclerosis, neointimal hyperplasia, stroke, hypertension, myocardial infarction, and heart failure. Across different cell types and pathological contexts, survivin plays a pivotal role throughout the disease progression-from the onset of disease development to the facilitation of compensatory mechanisms post-injury-primarily through its function in regulating cell proliferation and apoptosis. Furthermore, given the limited research on survivin as a therapeutic target for CVDs, potential clinical avenues, including YM155 (a survivin inhibitor) or adenoviral, adeno-associated, and lentiviral vectors, are also discussed. Overall, this review highlights survivin as a promising target for mitigating the detrimental effects of CVDs and to provide new perspectives to advance research on the intervention of CVDs and associated pathologies.

01 May 2025·International Journal of Biological Macromolecules

Integrative analysis of cuproptosis-related lncRNAs for prognostic risk assessment and tumor immune microenvironment evaluation in laryngeal squamous cell carcinoma

Article

Author: Deng, Haihua ; Zhao, Jiandong ; Xu, Haiming ; Wang, Cheng ; Qiu, Qibing ; Liu, Mingbo ; Zheng, Shikang ; Zhao, Kai ; Zhang, Rongqi ; Yang, Zhe

Long non-coding RNAs (lncRNAs) play a pivotal role in tumor prognostic models. This study targets cuproptosis-related lncRNAs in laryngeal squamous cell carcinoma (LSCC) using RNA-seq data from The Cancer Genome Atlas (TCGA)-LSCC. Differentially expressed genes were identified, and Pearson correlation analysis pinpointed cuproptosis-related lncRNAs. Combining clinical data, a prognostic risk model was constructed using LASSO Cox regression and Cox proportional hazards analyses. Nine lncRNAs (LINCO1473, SNHG12, AC007938.3, AC040970.1, AC023669.1, AL158166.2, GIHCG, AC007240.3, and AC011370.1) were identified, with GIHCG showing significant correlation with LSCC prognosis. GIHCG's competing endogenous RNAs (ceRNA) and co-expression networks (CEN) were established, revealing sensitivity to drugs like BMS-509744, YM155, and KU-55933. Silencing of GIHCG inhibited migration, invasion, EMT, and other biological processes in LSCC cells, suggesting GIHCG as a potential therapeutic target. Moreover, METTL16-mediated m6A methylation regulates GIHCG expression. In conclusion, this study successfully established a prognostic model comprising nine cuproptosis-related lncRNAs, accurately predicting LSCC prognosis, and highlighted the crucial role of GIHCG as a novel nucleic acid biomarker in regulating LSCC progression.

04 Apr 2025·Journal of Proteome Research

Multiomics Analysis Reveals Neuroblastoma Molecular Signature Predicting Risk Stratification and Tumor Microenvironment Differences

Article

Author: Qin, Xiaohan ; Wang, Jingyue ; Zhou, Xing ; Zhang, Da ; Zhou, Zhaokai ; Cheng, Jian ; Qin, Pan ; Fu, Yongcheng ; Wang, Yuanyuan

Neuroblastoma (NB) remains associated with high mortality and low initial response rate, especially for high-risk patients, thus warranting exploration of molecular markers for precision risk classifiers. Through integrating multiomics profiling, we identified a range of hub genes involved in cell cycle and associated with dismal prognosis and malignant cells. Single-cell transcriptome sequencing revealed that a subset of malignant cells, subcluster 1, characterized by high proliferation and dedifferentiation, was strongly correlated with the hub gene signature and orchestrated an immunosuppressive tumor microenvironment (TME). Furthermore, we constructed a robust malignant subcluster 1 related signature (MSRS), which was an independent prognostic factor and superior to other clinical characteristics and published signatures. Besides, TME differences conferred remarkably distinct therapeutic responses between high and low MSRS groups. Notably, polo-like kinase-1 (PLK1) was one of the most crucial contributors to MSRS and remarkably correlated with malignant subcluster 1, and PLK1 inhibition was effective for NB treatment as demonstrated by in silico analysis and in vitro experiments. Overall, our study constructs a novel molecular model to further guide the clinical classification and individualized treatment of NB.

1

News (Medical) associated with Sepantronium Bromide

19 Dec 2022

·www.biospace.com

Cothera Announces Dosing of First Patient in Phase 2 Clinical Trial to Test Its DUB Inhibitor PC-002 for the Treatment of High-Grade B-cell Lymphoma

San Francisco, December 19, 2022--Cothera Bioscience today announced that it has dosed the first patient with PC-002, a first-in-class deubiquitinase (DUB) inhibitor, in a global multi-center phase 2 clinical trial for the treatment of high-grade B-cell lymphoma with Myc rearrangement (NCT05263583). This is a single-arm, single-agent proof-of-concept trial designed to evaluate PC-002 in patients who are either resistant or refractory to prior treatments. The company also announced that a paper1 describing PC-002’s mechanism-of-action was accepted for publication in the European Journal of Pharmaceutical Science. PC-002 (also known as YM155, sepantronium bromide) is a first-in-class small molecule inhibitor of DUB, an enzyme family which removes ubiquitin from cellular proteins otherwise destined for degradation. By inhibiting a key DUB activity that stabilizes the Myc protein in cancer cells, PC-002 selectively induces Myc protein degradation and cell apoptosis in Myc-dependent tumors. As Myc is regarded as one of the most important yet “undruggable” cancer targets with increased expression in more than 50% of human cancers, PC-002 may potentially address multiple cancer indications involving Myc dysregulation. Dr. Alex Wu, Co-founder and CEO of Cothera Bioscience, commented: "We are excited to dose the first patient in this important proof-of-concept trial. DUBs are an emerging target family with broad potential in cancer and inflammation treatment. PC-002 is the most advanced clinical stage DUB inhibitor which works by accelerating the degradation of Myc oncoprotein and has great potential to treat cancers depending on high Myc activity. Myc-driven high-grade lymphoma is a highly malignant, life-threatening disease for which there is currently no good treatment. We look forward to validating the safety and efficacy of PC-002 through this trial, providing a new solution for improving the prognosis of patients with this devastating disease, and delivering a breakthrough in the treatment of Myc-driven tumors.” 1. Li et al. YM155 Inhibits Neuroblastoma Growth through Degradation of MYCN: A New Role as a USP7 Inhibitor, European Journal of Pharmaceutical Sciences (2022) doi: About Cothera Bioscience, Inc. Cothera Bioscience is a clinical stage biotech company developing therapeutics for previously undruggable oncology targets with high unmet medical needs. The company’s strength is in its clinically validated translational platform exploiting synthetic lethality and protein degradation pathways for cancer killing. It was formed by the core founding members of Crown Bioscience, a leading contract research organization specializing in translational oncology, together with veteran serial entrepreneurs from Silicon Valley. Proprietary i-CR® technology platform Cothera Bioscience developed a patented proprietary i-CR® technology platform, a powerful method for individualized drug screening and new drug development. The platform combines a high content screening system with conditional reprogramming of primary cultured tumor cells, which enables efficient and undifferentiated expansion of primary patient-derived tumor cells in vitro while preserving the tumor’s heterogeneity. Through collaboration with leading oncology medical centers, Cothera Bioscience carried out prospective clinical trials and demonstrated that the i-CR® system can effectively predict the actual clinical response of a drug, with potential to significantly improve the clinical efficacy and success rate in anticancer drug development. (Transl Oncol. 2021 Jan;14(1):100935). For more information, please visit or send email to: bd@cotherabio.com

Phase 2

100 Deals associated with Sepantronium Bromide

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KEGG	Wiki	ATC	Drug Bank
D10164	-	-	-

R&D Status

10 top R&D records.

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Indication	Highest Phase	Country/Location	Organization	Date
Diffuse large B-cell lymphoma refractory	Phase 3	United States	Astellas Pharma, Inc.	01 Jun 2007
Diffuse large B-cell lymphoma refractory	Phase 3	Canada	Astellas Pharma, Inc.	01 Jun 2007
Diffuse large B-cell lymphoma refractory	Phase 3	Spain	Astellas Pharma, Inc.	01 Jun 2007

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Clinical Result

Indication

Phase

Evaluation

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT05263583 (ASH2023)	Phase 2	C-Myc positive High grade B-cell lymphoma	-	PC-002 (Sepantronium Bromide, or SepB)	(zyazgjjwmr) = jynlsffcoa nhbhftgewu (pyzberzoay )	-	09 Dec 2023
NCT01007292 (Pubmed \| Leukemia) Manual	Phase 2	Aggressive B-Cell Non-Hodgkin Lymphoma	41	YM155+Rituximab	(ukxzgidaom) = jkqbchspzp zszbbzldfg (tkclcxdcnc ) View more	Negative	01 Aug 2016
ASCO2016	Phase 1	EGFR-mutated non-small Cell Lung Cancer	18	YM155 + Erlotinib	zskycdsnwt(pstphxpbds) = One patient receiving 4.8 mg/ m2/d Y developed a dose-limiting transient reversible grade 2 serum creatinine elevation mjjwagfodh (sdwssfbekq ) View more	Positive	20 May 2016
NCT01009775 (Pubmed \| Cancer Med) Manual	Phase 2	Melanoma	64	docetaxel+YM155	(lslwvtdsbk) = bdgclhtsiv cuhcrcmhoj (qsljgdfvag, 21.3 - 48.6) View more	Negative	01 May 2015
NCT01100931 (Pubmed \| Ann Oncol)	Phase 1/2	Advanced Lung Non-Small Cell Carcinoma	42	Sepantronium Bromide	(wyojixudby) = deshdzlvtb qefcvfopha (yvjxomxbku ) View more	-	01 Oct 2013
NCT01038804 (ASCO2013) Manual	Phase 2	HER2-negative breast cancer First line HER2 negative	101	docetaxel+YM155	(jusmxilprs) = fzvfpechqv kciegxouri (msrokuufcq, 176 - 333) View more	Positive	20 May 2013
NCT01038804 (ASCO2013) Manual	Phase 2	HER2-negative breast cancer First line HER2 negative	101	docetaxel	(jusmxilprs) = ryhscfrpzn kciegxouri (msrokuufcq, 202 - 433) View more	Positive	20 May 2013
ASCO2012	Phase 2	Melanoma	64	YM155 plus docetaxel	(qnretdcwst) = nlxxqjvutf nylyhumfxo (wgokfmnotv ) View more	Negative	20 May 2012
E1611 (ASCO2012)	Not Applicable	Merkel Cell Carcinoma	-	YM155	fdryergdsd(jrlngoiwnb) = qogvkitxgi wrgiwzxfvi (wkqjljztfy )	-	20 May 2012
E1611 (ASCO2012)	Not Applicable	Merkel Cell Carcinoma	-	Bortezomib	fdryergdsd(jrlngoiwnb) = jwxmpjjcbv wrgiwzxfvi (wkqjljztfy )	-	20 May 2012
ASCO2011	Phase 1	Solid tumor	22	Paclitaxel	(awzmjiuimd) = vbsnkmewib tkqcmaizkb (nilksbmvwb ) View more	-	20 May 2011
ASCO2011	Phase 1	Solid tumor	22	Carboplatin	(awzmjiuimd) = jolauupins tkqcmaizkb (nilksbmvwb ) View more	-	20 May 2011
ASCO2009	Not Applicable	Diffuse Large B-Cell Lymphoma	43	YM155	(apsldrxakz) = hpqihkelsc hrxstsbljs (suqkeurrjz ) View more	-	20 May 2009