Anygen Co.

South Korea

Anygen Co.

South Korea
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Patent
Anygen Co. | Date: 2017-01-25

The present invention relates to a novel exenatide analogue, which is an exenatide analogue in which the first to fifteenth amino acids from the C-terminal of the amino acid sequence of exenatide are deleted and a fatty acid is conjugated. The present invention provides a short length exenatide exhibiting almost the same level of anti-diabetic effects compared with that of conventional exenatide and liraglutide, which is an anti-diabetic drug, and capable of reducing the preparation cost of exenatide.


Patent
ANYGEN Co. | Date: 2015-03-23

The present invention relates to a novel exenatide analogue, which is an exenatide analogue in which the first to fifteenth amino acids from the C-terminal of the amino acid sequence of exenatide are deleted and a fatty acid is conjugated. The present invention provides a short length exenatide exhibiting almost the same level of anti-diabetic effects compared with that of conventional exenatide and liraglutide, which is an anti-diabetic drug, and capable of reducing the preparation cost of exenatide.


Ahn M.-Y.,Wonkwang University | Kim T.-H.,Sungkyunkwan University | Kwon S.-M.,Wonkwang University | Yoon H.-E.,Wonkwang University | And 8 more authors.
European Journal of Pharmaceutical Sciences | Year: 2015

This study examined the anti-tumor effects of AGM130, a novel indirubin-3′-oxime derivative in A549 human non-small cell lung cancer cells. AGM130 significantly inhibited the proliferation and arrested the cell cycle of G2/M phase. Induction of apoptosis was detected in AGM130-treated A549 cells. The protein levels of Cytochrome c release, Bax, cleaved caspases and PARP were increased in AGM130 treated cells, whereas Bcl-2 levels were decreased. AGM130 inhibited Insulin-like growth factor 1 receptor (IGF1R), AKT/mTOR signaling and inactivated mitogen-activated protein kinases (MAPK). AGM130 also induced slight autophagy as pro-survival function and autophagy inhibition by chloroquine (CQ) induced necrosis. In vivo tumor xenograft model, AGM130 dose-dependently suppressed transplanted A549 cell tumor growth and induced the expression of proliferative cell nuclear antigen (PCNA). AGM130 also increased TUNEL positive apoptotic cell populations and the induction of glandular differentiation with mucin pool compared with vehicle-treated control in tumor tissue. These results suggest that AGM130 is an effective novel indirubin-3′-oxime derivative of anti-cancer drug and may be an attractive candidate for non-small cell lung cancer therapy. © 2015 Elsevier B.V. All rights reserved.


Park W.-S.,Seoul St Marys Hospital | Park W.-S.,Catholic University of Korea | Park G.-J.,Seoul St Marys Hospital | Park G.-J.,Catholic University of Korea | And 12 more authors.
Cancer Chemotherapy and Pharmacology | Year: 2017

Purpose: AGM-130 is a cyclin-dependent kinase inhibitor that exhibits dose-dependent efficacy in xenograft mouse models. During preclinical pharmacokinetic (PK) studies, mice and rats showed comparable PK parameters while dogs showed unusually high clearance (CL), which has made human PK prediction challenging. To address this discrepancy, we performed a human microdosing PK and developed a mouse PK/PD model in order to guide the first-in-human studies. Methods: A microdose of AGM-130 was given via intravenous injection to healthy subjects. Efficacy data obtained using MCF-7 breast cancer cells implanted in mice was analyzed using pre-existing tumor growth inhibition models. We simulated a human PK/PD profile with the PK parameters obtained from the microdose study and the PD parameters estimated from the xenograft PK/PD model. Results: The human CL of AGM-130 was 3.08 L/h/kg, which was comparable to CL in mice and rats. The time-courses of tumor growth in xenograft model was well described by a preexisting model. Our simulation indicated that the human doses needed for 50 and 90% inhibition of tumor growth were about 100 and 400 mg, respectively. Conclusions: This is the first report of using microdose PK and xenograft PK/PD model to predict efficacious doses before the first-in-human trial in cancer patients. In addition, this work highlights the importance of integration of all of information in PK/PD analysis and illustrates how modeling and simulation can be used to add value in the early stages of drug development. © 2017, Springer-Verlag GmbH Germany.


Park M.-H.,Chungnam National University | Lee Y.Y.,Chung - Ang University | Lee Y.Y.,Bio Core Ltd | Cho K.H.,Bio Core Ltd | And 11 more authors.
Biomedical Chromatography | Year: 2016

A liquid chromatography-triple quadrupole mass spectrometric (LC-MS/MS) method was developed and validated for the determination of 5-nitro-5′-hydroxy-indirubin-3′-oxime (AGM-130) in human plasma to support a microdose clinical trial. The method consisted of a liquid-liquid extraction for sample preparation and LC-MS/MS analysis in the positive ion mode using TurboIonSprayTM for analysis. d3-AGM-130 was used as the internal standard. A linear regression (weighted 1/concentration) was used to fit calibration curves over the concentration range of 10-2000 pg/mL for AGM-130. There were no endogenous interference components in the blank human plasma tested. The accuracy at the lower limit of quantitation was 96.6% with a precision (coefficient of variation, CV) of 4.4%. For quality control samples at 30, 160 and 1600 pg/mL, the between run CV was ≤5.0 %. Between-run accuracy ranged from 98.1 to 101.0%. AGM-130 was stable in 50% acetonitrile for 168 h at 4°C and 6 h at room temperature. AGM-130 was also stable in human plasma at room temperature for 6 h and through three freeze-thaw cycles. The variability of selected samples for the incurred sample reanalysis was ≤12.7% when compared with the original sample concentrations. This validated LC-MS/MS method for determination of AGM-130 was used to support a phase 0 microdose clinical trial. © 2016 John Wiley & Sons, Ltd.


Choi S.-J.,Gwangju Institute of Science and Technology | Lee J.-E.,Gwangju Institute of Science and Technology | Jeong S.-Y.,Anygen Co. | Im I.,Gwangju Institute of Science and Technology | And 11 more authors.
Journal of Medicinal Chemistry | Year: 2010

To enhance the ability of indirubin derivatives to inhibit CDK2/cyclin E, a target of anticancer agents, we designed and synthesized a new series of indirubin-3′-oxime derivatives with combined substitutions at the 5 and 5′ positions. A molecular docking study predicted the binding of derivatives with OH or halogen substitutions at the 5′ position to the ATP binding site of CDK2, revealing the critical interactions that may explain the improved CDK2 inhibitory activity of these derivatives. Among the synthesized derivatives, the 5-nitro-5′-hydroxy analogue 3a and the 5-nitro-5′-fluoro analogue 5a displayed potent inhibitory activity against CDK2, with IC50 values of 1.9 and 1.7 nM, respectively. These derivatives also showed antiproliferative activity against several human cancer cell lines, with IC50 values of 0.2-3.3 μM. A representative analogue, 3a, showed greater than 500-fold selectivity for CDK relative to selected kinase panel and potent in vivo anticancer activity. © 2010 American Chemical Society.


Patent
Anygen Inc., Samsung, Snu R&D Foundation and Chonbuk National University | Date: 2016-01-13

The present invention relates to a pharmaceutical composition for treating or preventing erectile dysfunction, containing LDD175 as an active ingredient. Furthermore, the present invention relates to a co-administration preparation for treating or preventing erectile dysfunction, containing LDD175 and a PDE5 inhibitor as active ingredients. The LDD175 of the present invention has an excellent corporal smooth muscle relaxation effect, and thus significantly improved erectile function. Since the LDD175 of the present invention acts on BK_(Ca )channels, and thus is expected to have little adverse cardiovascular effects. The LDD175 of the present invention exhibits an erectile dysfunction therapeutic ability equivalent to that of udenafil, which is a PDE5 inhibitor, and showed a synergistic corporal smooth muscle relaxation effect when being co-administered with udenafil.


Patent
Anygen Co. | Date: 2014-05-23

Provided is a conjugate including a pharmacologically active substance covalently bound to chitosan or its derivative and a method for transmucosal delivery of a pharmacologically active substance using the same. Specifically a conjugate includes a pharmacologically active substance covalently bound via a linker to chitosan; and a pharmaceutical composition for transmucosal administration of a drug includes the aforementioned conjugate and a pharmaceutically acceptable carrier. Further provided is a method for in vivo delivery of a pharmacologically active substance via a transmucosal route, by covalent binding of the active substance with chitosan or its derivative via a linker. The conjugate in accordance with the present invention exhibits excellent absorption rate and biocompatibility in biological mucous membranes, particularly mucous membranes of the alimentary canal (especially the gastrointestinal tract), in vivo degradability, and superior bioavailability even with oral administration, thus enabling treatment of diseases via oral administration of a drug.


The present invention relates to a composition for regulating circadian rhythms, a composition for diagnosing circadian rhythm disorders and a diagnostic kit, wherein the composition for regulating circadian rhythms comprises NQ peptides, C12orf39 genes, NQ peptides cDNA and the like, which relate to circadian regulation in vertebrates as main components.


The present invention relates to an indirubin-3-oxime derivative as potent cyclin dependent kinase inhibitor with anti-cancer activity. More particularly, this invention relates to an indirubin-3-oxime derivative as potent cyclin dependent kinase inhibitor having excellent anti-cancer activity against human lung cancer cell, human fibro sarcoma cell, human colon cancer cell, human leukemia cell, human stomach cancer cell, human nasopharyngeal cancer cell and/or human breast cancer cell.

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