Delving into the Latest Updates on ProChon Biotech Ltd. with Synapse

Phase II Study to Investigate the Efficacy and Safety of BioCart™II in the Treatment of Symptomatic Cartilage Defects of the Femoral Condyle in Comparison With Microfracture

BioCart™II is a novel scaffold seeded with autologous chondrocytes to be used to repair cartilage lesions of the knee. This study is designed to compare the efficacy and safety of BioCart™II treatment compared to microfracture which is the classical method of treatment.

开始日期2008-05-01

申办/合作机构

ProChon Biotech Ltd.

100 项与 ProChon Biotech Ltd. 相关的临床结果

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0 项与 ProChon Biotech Ltd. 相关的专利（医药）

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8

项与 ProChon Biotech Ltd. 相关的文献（医药）

2011-01-01·CARTILAGE3区 · 医学

The Chondrogenic Potential of Mesenchymal Cells and Chondrocytes from Osteoarthritic Subjects

3区 · 医学

Article

作者: Blumenstein, Sara ; Fischler, Tali ; Agar, Gabriel ; Yayon, Avner ; Kardosh, Rami ; Goldschmid, Revital ; Gal-Levy, Ronit ; Schrift-Tzadok, Michal ; Bar-Ziv, Yaron

Objective: The multipotential nature of stem or progenitor cells apparently makes them the ideal choice for any cell therapy, but this as yet remains to be proven. This study (30 subjects) was designed to compare the potential to repair articular cartilage of chondrocytes taken from different regions in osteoarthritic cartilage with that of mesenchymal stem cells prepared from bone marrow of the same subject. Design: Cartilage biopsies, bone marrow, and blood samples were taken from each of 30 individuals with chronic osteoarthritis (aged 62-85 years) undergoing total knee replacement. The chondrogenic potential of chondrocytes isolated from cartilage biopsies taken from different regions of osteoarthritic cartilage was compared with that of mesenchymal cells by quantitative analysis of several chondrocyte specific markers and an ex vivo cartilage differentiation assay. Results: Cartilage-derived articular chondrocytes are superior to bone marrow–derived cells when compared for their ex vivo chondrogenic potential. Interestingly, there was marked and significant difference in the expression of chondrocytic markers between chondrocytes derived from adjacent, visually distinct regions of the diseased cartilage. When cultured in the presence of a fibroblast growth factor 2 variant, all cell samples from both tissues showed a high degree of chondrogenic potential. Conclusions: Although bone marrow–derived mesenchymal cells, when supplemented with the appropriate chondrogenic factors, are a suitable source for autologous cartilage implantation, adult chondroprogenitor cells, particularly those from moderately affected regions of the osteoarthritic joints, demonstrate superior chondrogenic potential.

2008-03-01·Stem Cells2区 · 医学

Fibroblast Growth Factor 4 and Its Novel Splice Isoform Have Opposing Effects on the Maintenance of Human Embryonic Stem Cell Self-Renewal

2区 · 医学

Article

作者: Benvenisty, Nissim ; Yayon, Avner ; Chumakov, Irina ; Rom, Eran ; Mayshar, Yoav ; Kronman, Achia

AbstractHuman embryonic stem cells (HESCs) are unique in their capacity to self-renew while remaining pluripotent. This undifferentiated state must be actively maintained by secreted factors. To identify autocrine factors that may support HESC growth, we have taken a global genetic approach. Microarray analysis identified fibroblast growth factor 4 (FGF4) as a prime candidate for autocrine signaling. Furthermore, the addition of recombinant FGF4 to HESCs supports their proliferation. We show that FGF4 is produced by multiple undifferentiated HESC lines, along with a novel fibroblast growth factor 4 splice isoform (FGF4si) that codes for the amino-terminal half of FGF4. Strikingly, although FGF4 supports the undifferentiated growth of HESCs, FGF4si effectively counters its effect. Furthermore, we show that FGF4si is an antagonist of FGF4, shutting down FGF4-induced Erk1/2 phosphorylation. Expression analysis shows that both isoforms are expressed in HESCs and early differentiated cells. However, whereas FGF4 ceases to be expressed in mature differentiated cells, FGF4si continues to be expressed after cell differentiation. Targeted knockdown of FGF4 using small interfering RNA increased differentiation of HESCs, demonstrating the importance of endogenous FGF4 signaling in maintaining their pluripotency. Taken together, these results suggest a growth-promoting role for FGF4 in HESCs and a putative feedback inhibition mechanism by a novel FGF4 splice isoform that may serve to promote differentiation at later stages of development.Disclosure of potential conflicts of interest is found at the end of this article.

2003-07-01·Current Drug Targets4区 · 医学

Fibroblast Growth Factor Receptor-3 as a Therapeutic Target for Achondroplasia - Genetic Short Limbed Dwarfism

4区 · 医学

Review

作者: Golembo, Myriam ; Aviezer, David ; Yayon, Avner

Achondroplasia, the most common form of human dwarfism is a sporadic autosomal dominant condition that occurs in approximately 1:20,000 births. The major clinical outcome of Achondroplasia is attenuated growth, rhizomelic shortening of the long bones and craniofacial abnormalities. As of today there is no pharmacological treatment for Achondroplasia. Some improvement in the patients well being and daily function can be achieved by a surgical limb lengthening procedure. Growth hormone treatment seems to have only modest short term success and to lack long term benefits. Achondroplasia results from a single point mutation in Fibroblast Growth Factor Receptor 3 (FGFR3). In 97% of the patients, there is a Glycine to Arginine substitution at position 380 within the FGFR-3 transmembrane domain leading to receptor overactivation. This FGF receptor tyrosine kinase is expressed by chondrocytes in the growth plate of developing long bones and plays a crucial role in bone growth. Genetic disruption of the FGFR-3 gene in mice leads to a remarkable increase in the length of the vertebral column and long bones. This suggests that overaction of FGFR3 signaling may specifically impair chondrocyte function within the epiphyseal growth plates and cause Achondroplasia. Reconstituted normal bone growth may therefore be achieved by attenuation of FGFR3 signaling in the appropriate cells within the growth plate. It is highly conceivable that drug development strategies aimed either towards blocking extracellular ligand binding or towards intracellular checkpoints along the FGF signal transduction cascade, may prove successful in the treatment of Achondroplasia. This review focuses on the possible approaches for developing a drug for Achondroplasia and related skeletal disorders, using chemical, biochemical and molecular strategies.

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