Phase I, Randomized, Multicenter, Double-blind, Single Dose, Dose-Escalation, Placebo-Controlled, Parallel Group Clinical Trial to Investigate the Safety, Tolerability and Pharmacokinetics of Intravenous Administration of Cardiotrophin-1 (CT-1)in Healthy Volunteers

The general aim of the study is to determinate safety, tolerability and early pharmacokinetics of cardiotrophin.1 in healthy volunteers.

Start Date01 Nov 2012

Sponsor / Collaborator

Digna Biotech SL

100 Clinical Results associated with Cardiotrophin-1(Biotecnol Ltd.)

100 Translational Medicine associated with Cardiotrophin-1(Biotecnol Ltd.)

100 Patents (Medical) associated with Cardiotrophin-1(Biotecnol Ltd.)

142

Literatures (Medical) associated with Cardiotrophin-1(Biotecnol Ltd.)

01 Jan 2025·Cell Reports Medicine

Dual ferroptosis induction in N2-TANs and TNBC cells via FTH1 targeting: A therapeutic strategy for triple-negative breast cancer

Article

Author: Lin, Jiayi ; Sun, Qingyan ; Chen, Hongzhuan ; Zhang, Lijun ; Yan, Yue ; Luan, Xin ; Yan, Li ; Jin, Jinmei ; Liu, Yichen ; Gong, Yiting ; Yuan, Hu ; Guo, Jingwen ; Wang, Bei ; Zhang, Weidong

Tumor-associated neutrophils (TANs) play a critical role in the progression and prognosis of triple-negative breast cancer (TNBC), with N2-type TANs known for their pro-tumor characteristics. This study introduces CT-1, a derivative of cryptotanshinone that effectively suppresses TNBC growth while selectively reducing the proportion of N2-type TANs within tumor tissue. Notably, CT-1 induces simultaneous ferroptosis in both N2-type TANs and TNBC cells, a dual mechanism that enhances its therapeutic efficacy. The study identifies ferritin heavy chain 1 (FTH1), a key protein in iron metabolism, as the direct target of CT-1. By targeting FTH1, CT-1 facilitates the interaction between NCOA4 and ferritin, triggering ferritinophagy-mediated ferroptosis. These findings position CT-1 as a promising therapeutic agent, offering a strategy to combat TNBC by inducing ferroptosis in both N2-type TANs and cancer cells. This approach underscores the potential of FTH1 as a therapeutic target for treating TNBC.

01 Jul 2024·Physiological Reports

Cardiotrophin‐1 therapy reduces disease severity in a murine model of glomerular disease

Article

Author: Kolatsi‐Joannou, Maria ; Jafree, Daniyal J. ; Long, David A. ; Pomeranz, Gideon ; Perretta‐Tejedor, Nuria ; Vasilopoulou, Elisavet ; Martínez‐Salgado, Carlos ; Price, Karen L.

AbstractCardiotrophin‐1 (CT‐1), a member of the interleukin (IL)‐6 cytokine family, has renoprotective effects in mouse models of acute kidney disease and tubulointerstitial fibrosis, but its role in glomerular disease is unknown. To address this, we used the mouse model of nephrotoxic nephritis to test the hypothesis that CT‐1 also has a protective role in immune‐mediated glomerular disease. Using immunohistochemistry and analysis of single‐cell RNA‐sequencing data of isolated glomeruli, we demonstrate that CT‐1 is expressed in the glomerulus in male mice, predominantly in parietal epithelial cells and is downregulated in mice with nephrotoxic nephritis. Furthermore, analysis of data from patients revealed that human glomerular disease is also associated with reduced glomerular CT‐1 transcript levels. In male mice with nephrotoxic nephritis and established proteinuria, administration of CT‐1 resulted in reduced albuminuria, prevented podocyte loss, and sustained plasma creatinine, compared with mice administered saline. CT‐1 treatment also reduced fibrosis in the kidney cortex, peri‐glomerular macrophage accumulation and the kidney levels of the pro‐inflammatory mediator complement component 5a. In conclusion, CT‐1 intervention therapy delays the progression of glomerular disease in mice by preserving kidney function and inhibiting renal inflammation and fibrosis.

01 Aug 2023·Theriogenology

Conjugated linoleic acid supplementation changes prostaglandin concentration ratio and alters the expression of genes involved in maternal-fetal recognition from bovine trophoblast cells in vitro

Article

Author: Pugliesi, Guilherme ; Mendes, Adriano Felipe ; Ealy, Alan D ; Nogueira, Marcelo Fábio Gouveia ; Feltrin, Isabella Rio ; de Castro Lourenço, Valeska ; de Oliveira Bezerra, Lucas ; Rocha, Cecilia Constantino ; Membrive, Claudia Maria Bertan ; Bueno Cordeiro Maldonado, Mariângela

Early embryonic mortality caused by maternal-fetal recognition failure in the three weeks after fertilization represents a major cause of reproductive inefficiency in the cattle industry. Modifying the amounts and ratios of prostaglandin (PG) F_2α and PGE₂ can benefit the establishment of pregnancy in cattle. Adding conjugated linoleic acid (CLA) to endometrial and fetal cells culture affects PG synthesis, but its effect on bovine trophoblast cells (CT-1) is unknown. The aim of this study was to determine the effects of CLA (a mixture of cis- and trans-9, 11- and -10,12-octadecadienoic acids) on PGE₂ and PGF_2α synthesis and the expression of transcripts involved with maternal-fetal recognition of bovine trophectoderm. Cultures of CT-1 were exposed to CLA for 24, 48 and 72 h. Transcript abundance was determined by qRT-PCR and hormone profiles were quantified by ELISA. The PGE₂ and PGF_2α concentrations were reduced in the culture medium of CLA-exposed CT-1 compared to that of unexposed cells. Furthermore, CLA supplementation increased the PGE₂:PGF_2α ratio in CT-1 and had a quadratic effect (P < 0.05) on the relative expression of MMP9, PTGES2, and PTGER4. The relative expression levels of PTGER4 were reduced (P < 0.05) in CT-1 cultured with 100 μM CLA than in the unsupplemented and 10 μM-CLA groups. Treatment of CT-1 with CLA decreased PGE₂ and PGF_2α synthesis but a biphasic effect of CLA was observed on the PGE₂:PGF_2α ratio and relative abundance of transcripts with 10 μM CLA providing maximal improvements in each endpoint. Our data suggest that CLA may influence eicosanoid metabolic process and extracellular matrix remodeling.

100 Deals associated with Cardiotrophin-1(Biotecnol Ltd.)

R&D Status

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Indication	Highest Phase	Country/Location	Organization	Date
Myocardial Reperfusion Injury	Phase 2	-	Biotecnol Ltd.Startup	-
Myocardial Reperfusion Injury	Phase 2	-	Digna Biotech SL	-
Myocardial Reperfusion Injury	Phase 2	-	Genentech, Inc.	-
Acute Kidney Injury	Phase 1	-	Digna Biotech SL	-
Acute Kidney Injury	Phase 1	-	Genentech, Inc.	-
Acute Kidney Injury	Phase 1	-	Biotecnol Ltd.Startup	-
Huntington Disease	Preclinical	United States	Microbot Medical, Inc.	-
liver function failure	Preclinical	-	Genentech, Inc.	-
liver function failure	Preclinical	-	Biotecnol Ltd.Startup	-
liver function failure	Preclinical	-	Digna Biotech SL	-

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