PIPELINE

Renaissance of Medicine

PIPELINE

Renaissance of Medicine

MDC-101
Gene Therapy for Avellino Corneal Dystrophy

Anti-sense oligonucleotide for targeting mutant TGFBI R124H mRNA which causes the precipitation of mutant TGFBI and corneal turbidity

Progress in Retinal and Eye Research 50 (2016) 67-88


Avellino corneal dystrophy (ACD) is a serious ophthalmic genetic disorder that causes corneal opacity through a specific mutation in transforming growth factor beta-induced gene (TGFBI) and ultimately leads to blindness. The R124H mutation in TGFBI protein is considered as the disease causing mutation, and appears in 1/870 of Korean population and half of that in the global population. However, no treatment of ACD is approved to date. Our RNAi technology facilitates the selective targeting of the R124H driver mutation of TGFBI at mRNA level, circumventing the off-target effects and enhancing the therapeutic efficacy.

MDC-201
Therapy for Fuchs Endothelial Corneal Dystrophy

Multi-functional therapeutics for the treatment of ROS-induced oxidation and TGF-β-induced fibrosis in Fuchs Corneal Dystrophy

N Engl J Med 363 (2010) 1016-1024

Fuchs endothelial corneal dystrophy (FECD) is a corneal disease with corneal edema, opacity, and visual impairment, caused by deformation and damage of corneal endothelial cells as a result of factors such as UV and oxidative stress. The prevalence of FECD is estimated to be 4~6% in people over the age of 50, and the disease imparts multiple underlying mechanisms and complex pathophysiology. To date, FECD is the main ophthalmic disease requiring corneal transplant surgery, and currently only surgical procedures such as keratectomy are applicable to FECD patients. Our novel FECD treatment strategy suggests blocking both intrinsic and extrinsic pathogenic mechanisms of oxidative stress and fibrosis, and therefore provides effective treatment option for complex FECD pathophysiology.

MDC-202
Therapy for Myelodysplastic Syndrome

Novel oral hypomethylation agent for the treatment of incurable drug-resistant myelodysplastic syndrome

Myelodysplastic syndrome (MDS) is bone marrow disease characterized by the abnormal production of immature blood cells, and has a high risk of developing into acute myeloid leukemia. Hypomethylation agent (Azacitidine or Decitabine) is currently recommended as the standard therapy for higher MDS; yet, the adapted hypomethylation agent-resistance in over 50% patients becomes a recurrent clinical problem in treating MDS. MediciBIO develops a novel oral hypomethylation agent that overcomes the current drug-resistance, and aims to improve patient convenience of medication as well as therapeutic outcomes of MDS patients. 

MDC-101: Gene Therapy for Avellino Corneal Dystrophy

Avellino corneal dystrophy (ACD) is a serious ophthalmic genetic disorder that causes corneal opacity through a specific mutation in transforming growth factor beta-induced gene (TGFBI) and ultimately leads to blindness. The R124H mutation in TGFBI protein is considered as the disease causing mutation, and appears in 1/870 of Korean population and half of that in the global population. However, no treatment of ACD is approved to date. Our oligonucleotide drug technology facilitates the selective targeting of the R124H driver mutation of TGFBI at mRNA level, circumventing the off-target effects and enhancing the therapeutic efficacy.

MDC-201 : Therapy for Fuchs Endothelial Corneal Dystrophy

Fuchs endothelial corneal dystrophy (FECD) is a corneal disease with corneal edema, opacity, and visual impairment, caused by deformation and damage of corneal endothelial cells as a result of factors such as UV and oxidative stress. The prevalence of FECD is estimated to be 4~6% in people over the age of 50, and the disease imparts multiple underlying mechanisms and complex pathophysiology. To date, FECD is the main ophthalmic disease requiring corneal transplant surgery, and currently only surgical procedures such as keratectomy are applicable to FECD patients. Our novel FECD treatment strategy suggests blocking both intrinsic and extrinsic pathogenic mechanisms of oxidative stress and fibrosis, and therefore provides effective treatment option for complex FECD pathophysiology.

MDC-202 : Therapy for Myelodysplastic Syndrome

Myelodysplastic syndrome (MDS) is bone marrow disease characterized by the abnormal production of immature blood cells, and has a high risk of developing into acute myeloid leukemia. Hypomethylation agent (Azacitidine or Decitabine) is currently recommended as the standard therapy for higher MDS; yet, the adapted hypomethylation agent-resistance in over 50% patients becomes a recurrent clinical problem in treating MDS. MediciBIO develops a novel oral hypomethylation agent that overcomes the current drug-resistance, and aims to improve patient convenience of medication as well as therapeutic outcomes of MDS patients.

Addressㅣ  A-2207, 184, Jungbu-daero, Giheung-gu, Yongin-si, 

                    Gyeonggi-do, 17095 Republic of Korea

Telㅣ  +82-31-895-6707    Faxㅣ  +82-70-8676-6706

Copyright © MediciBIO Co.,LTD. All rights reserved. 

Headquarter   A-2207, 184, Jungbu-daero, Giheung-gu, Yongin-si, Gyeonggi-do, 17095 Republic of Korea

Branch Office  A-13, 3rd Floor, 194-25, Osongsaengmyeong 1-ro, Osong-eup, Heungdeok-gu, Cheongju-si, Chungcheongbuk-do, 28160 Republic of Korea

Tel ㅣ +82-31-895-6707     Fax ㅣ +82-70-8676-6706    Email ㅣ biz@medicibio.com

Copyright © MediciBIO Co.,LTD. All rights reserved.