Delving into the Latest Updates on HPN-01 with Synapse

Overview

Basic Info

Drug Type

Small molecule drug

Synonyms

Target

SREBF1 x SREBP-2

Action

inhibitors

Mechanism

SREBF1 inhibitors(Sterol regulatory element binding transcription factor 1 inhibitors), SREBP-2 inhibitors(Sterol regulatory element-binding protein 2 inhibitors)

Therapeutic Areas

Digestive System Disorders

Active Indication

Nonalcoholic Steatohepatitis

Inactive Indication-

Originator Organization

Shanghai Hepuhua Pharmaceutical Technology Co Ltd

Active Organization

Shanghai Hepuhua Pharmaceutical Technology Co Ltd

Inactive Organization

Hepanova, Inc.Startup

Drug Highest PhasePhase 1

First Approval Date-

Regulation-

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Structure/Sequence

Molecular FormulaC19H16ClN3O3S

InChIKeyXJLFMRGTLRIXDT-UHFFFAOYSA-N

CAS Registry928655-63-4

主要目的：考察健康受试者单、多次口服给予HPN-01肠溶胶囊的安全性和耐受性；次要目的：评价健康受试者单、多次口服给予HPN-01肠溶胶囊的药代动力学特性；评价食物对健康受试者单次服用HPN-01肠溶胶囊后药代动力学特性的影响；

[Translation]

Main purpose: To investigate the safety and tolerability of HPN-01 enteric-coated capsules after single and multiple oral administration to healthy subjects; Secondary purpose: To evaluate the pharmacokinetic properties of HPN-01 enteric-coated capsules after single and multiple oral administration to healthy subjects; To evaluate the effect of food on the pharmacokinetic properties of HPN-01 enteric-coated capsules after single administration to healthy subjects;

Start Date23 Apr 2021

Sponsor / Collaborator

Shanghai Hepuhua Pharmaceutical Technology Co Ltd

NCT04481594

/ Unknown statusPhase 1

A Randomized, Double-Blind, Placebo Controlled, Sequential Parallel Group, Single and Multiple Ascending Doses (SAD/MAD) Study Following Oral Administration in Healthy Subjects to Evaluate the Safety, Tolerability, Pharmacokinetics and Pharmacodynamics of HPN-01

This study is a randomized, double-blind, placebo-controlled first-in-human study in which the safety, tolerability, pharmacokinetics and pharmacodynamics of orally administered HPN-01 will be evaluated in healthy subjects

Start Date08 Sep 2020

Sponsor / Collaborator

Hepanova, Inc.Startup

100 Clinical Results associated with HPN-01

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100 Translational Medicine associated with HPN-01

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100 Patents (Medical) associated with HPN-01

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8

Literatures (Medical) associated with HPN-01

01 May 2022·Arabian Journal of Chemistry

Identify promising IKK-β inhibitors: A docking-based 3D-QSAR study combining molecular design and molecular dynamics simulation

Author: Wu, Chunjie ; Liu, Yefang ; Xiong, Chan ; Wang, Jiaolong ; Peng, Chang'en ; Wang, Yonggang ; Li, Liang

Inhibitor of nuclear factor kappa B kinase subunit beta (IKK-β), a specific regulator of nuclear factor-κB (NF-κB), is considered a valid target to design novel drugs to treat rheumatoid arthritis, glomerulonephritis and various cancers.In this study, in order to design and then identify promising compounds targeting IKK-β, a series of reported IKK-β inhibitors were used to develop 3D-QSAR models.Docking-based and minimization-based poses were generated for model construction.CoMSIA model #8 based on docking poses was selected due to its satisfactory internal and external validation results and the sufficient information delivery capability.After a contour map anal., 41 new designs were depicted based on a graphical design scheme and 25 of them were assessed as eligible for screening.Compound 21MX007 has aroused our attention for its both competitive QSAR-prediction and docking-scoring result.Detailed docking interactions of 21MX007-protein complex were investigated via a deep anal. of docking results and a comparative mol. dynamics simulation.Strong interactions and an extra hydrogen bond which echoes the H-bond requirements of substituent acquired from the design scheme were observedFrom MD anal., 21MX007-protein system was tested.The system was proved to have good stability in terms of a downward trend of RMSD and Rg values and a continuous and stable H-bond interaction and a lower average binding free energy.Thus, compound 21MX007 was successfully identified as a promising IKK-β inhibitor.

01 Apr 2015·International ImmunopharmacologyQ2 · MEDICINE

Modulation of inflammatory response in mice with severe autoimmune disease by thymic peptide thymulin and an inhibitor of NF-kappaB signalling

Q2 · MEDICINE

Article

Author: Glushkova, O V ; Parfenyuk, S B ; Novoselova, T V ; Novoselova, E G ; Khrenov, M O ; Fesenko, E E ; Lunin, S M

To investigate some cellular and molecular aspects of the autoimmune response and anti-inflammatory efficiency of potential therapeutic agents in a severe form of experimental autoimmune encephalomyelitis (sEAE), an inhibitor of NF-kappaB signalling, IKK Inhibitor XII, and/or thymic peptide thymulin, were injected intraperitoneally at 1.8 and 0.15mg/kg e.o.d, respectively, to C57BL/6 mice immunized with myelin oligodendrocyte glycoprotein and several adjuvants. The immunization induced high lethality in three weeks. The biphasic cytokine response observed in earlier and delayed phases was attributed to the activity of Th1 and Th17 cells, respectively. Phosphorylation of RelA protein from the NF-kappaB family increased during the earlier phase and decreased in the delayed phase. SAPK/JNK signalling protein and heat shock protein Hsp72 significantly increased in lymphocytes. Both the IKK Inhibitor XII and thymulin reduced disease severity, attenuated immune imbalance, and increased mouse life-span. Co-administration of the agents produced no additive effect. Both the inhibitor and thymulin reduced the Th1 response but not the Th17 response. Therefore, RelA-associated Th1 activation and RelA-independent Th17 activation occurred in sEAE. Thymulin and the inhibitor demonstrate similar patterns of activity, potentially through the RelA pathway inhibition, resulting in a partial therapeutic effect on the animals' health status.

01 May 2012·Biophysics

Effects of several inhibitors of intracellular signaling on production of cytokines and signal proteins in RAW 264.7 cells cultivated with low dose ammonium

Author: T. V. Novoselova ; E. G. Novoselova ; E. E. Fesenko ; S. B. Parfenuyk ; O. V. Glushkova ; S. M. Lunin ; M. O. Khrenov

Effects of four inhibitors of NF-κB, SAPK/JNK and TLR4 signaling, namely, inhibitor XII, SP600125, CLI-095 and OxPAPC on a macrophage response to low dose ammonium were studied in RAW 264.7 cells.Low dose ammonium induced proinflammatory response in cells as judged from enhanced production of TNF-α, IFN-Γ, and IL-6, and by activation of signal cascades.The increase in production of cytokines, namely TNF, IFN, and IL-6, demonstrated that low-dose ammonium induced a proinflammatory cellular response.In addition, an activation of NF-κB and SAPK/JNK cascades, as well as enhancement of TLR4 expression was shown.Each of used inhibitors reduced to a variable degree the proinflammatory response of RAW 264.7 cells to chem. toxin by decreasing cytokine productionThe inhibitor of NF-κB cascade, IKK Inhibitor XII, was more effective, and not only prevented the development of proinflammatory response induced by ammonium, but also decreased cytokine production below control values.The inhibitor of extracellular domains of TLR2 and TLR4 (OxPAPC) had almost the same anti-inflammatory effect, and an addition of the inhibitor of JNK cascade (SP600125) to cell culture practically neutralized the effect of ammonium ions by decreasing cytokine production to control level.Inhibitor anal. showed that activation of RAW 264.7 cells induced by chem. toxin coincided incompletely with intracellular signaling pathways that were earlier determined regarding macrophage response to toxin from Gram-neg. bacteria.Nevertheless, application of the inhibitors protected RAW 264.7 from the toxic effect of low dose ammonium.

100 Deals associated with HPN-01

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