N-terminal fusion partner for producing recombinant polypeptide, and method for producing recombinant polypeptide using same

    公开(公告)号:US11267863B2

    公开(公告)日:2022-03-08

    申请号:US16963066

    申请日:2019-01-18

    申请人: PEPGENE INC.

    发明人: Sung Gun Kim

    摘要: Disclosed are a novel N-terminal fusion partner, a fusion polypeptide including the fusion partner and a target polypeptide, and a method for producing a target polypeptide using the same. The novel fusion partner can enhance the yield of a target polypeptide (recombinant polypeptide) compared to the conventional fusion partners. Using the novel fusion partner is particularly beneficial in producing a target polypeptide having a relatively low molecular weight and an easily degradable amino terminus based on genetic recombination technologies. Further, the novel fusion polypeptide including the fusion partner can be expressed as inclusion bodies in a host cell and protected against proteases or the like in a host cell, which makes the target polypeptide produced stably. Therefore, in comparison to the conventional fusion partners, the novel fusion partner can be used to provide a method for producing a recombinant peptide with improved stability and yield.

    Method of treating a vasculopathy in a human subject

    公开(公告)号:US11219668B2

    公开(公告)日:2022-01-11

    申请号:US15530196

    申请日:2015-05-01

    摘要: The present invention is based upon the observation that inhibition of NPR-C Signaling pathway leads to the development of pulmonary arterial hypertension (PAH). Accordingly, the invention provides a mouse model for PAH, and proposes a method of using synthetic analogs of the NPR-C signaling pathway, specifically synthetic C-type atrial natriuretic factor or intermediates for, or modulators of, the NPR-C signaling pathway as anti-pulmonary vasculopathy agents. Activators of the NPR-C signaling pathway are disclosed to treat or prevent vasculopathy, including but not limited to PAH and other types of pulmonary hypertension, peripheral vascular disease, critical limb ischemia, coronary artery disease, and diabetic vasculopathy.

    COMPOSITIONS COMPRISING ALKALINE PHOSPHATASE AND/OR NATRIURETIC PEPTIDE AND METHODS OF USE THEREOF

    公开(公告)号:US20180326019A1

    公开(公告)日:2018-11-15

    申请号:US16039991

    申请日:2018-07-19

    摘要: The present invention provides methods, compositions, and kits for the treatment of neurocutaneous syndromes, such as neurofibromatosis type I; disorders associated with overactivation of FGFR3, such as achondroplasia; bone or cartilage disorders; or vascular smooth muscle disorders; or for the elongation of bone. In some embodiments, the present invention provides polypeptides having an alkaline phosphatase peptide fused to an Fc domain of an immunoglobulin or a natriuretic peptide fused to an Fc domain of an immunoglobulin. Such polypeptides can be administered to subjects, e.g., subcutaneously, to treat a neurocutaneous syndrome, a disorder associated with overactivation of FGFR3, a bone or cartilage disorder, or a vascular smooth muscle disorder, or to elongate bone. The invention also features nucleic acid molecules encoding such polypeptides and the use of the nucleic acid molecules for treating neurocutaneous syndromes, disorders associated with overactivation of FGFR3, bone or cartilage disorders, or vascular smooth muscle disorders, or for elongating bone.

    Method of treating skeletal dysplasias using vessel dilator

    公开(公告)号:US09956267B2

    公开(公告)日:2018-05-01

    申请号:US14757770

    申请日:2015-12-23

    申请人: David Lynn Vesely

    发明人: David Lynn Vesely

    摘要: C-natriuretic peptide (CNP) has been shown to regulate proliferation of mouse and rat osteoblasts. Genetic deletion of CNP results in dwarfism. CNP effects on bone growth involve inhibition of MEK 1 and ERK 1/2 kinases mediated via the intracellular messenger cyclic GMP. Vessel dilator is another natriuretic peptide synthesized by the atrial natriuretic peptide gene whose biologic half-life is 12 times longer than CNP. Vessel dilator's biologic effects on proliferating cells are mediated via inhibiting MEK 1/2 and ERK 1/2 kinases via cyclic GMP. Vessel dilator was not studied previously on osteoblasts. CNP and vessel dilator were tested in dose-response studies enhanced human osteoblasts' proliferation, showing that vessel dilator has identical mechanisms of action to CNP but much longer biologic half-life and effects at lower concentrations. Vessel dilator exhibited therapeutic effect for use in human achondroplasia, short stature and osteoporosis by stimulating osteoblast proliferation.