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Emil Tsai, Chief Executive Officer, SyneuRx International (Taiwan) Corp

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. Incremental success can lead to paradigm shift in CNS drug discovery

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Minimizing placebo responses

• Clinician training

 Understand placebo responses

 Do¡¦s and Don¡¦ts training to minimize physician cues that might induce placebo responses

 Script of honest answers to the assessment interview

Optimizing signal-to-noise in assessing patient responses

• Proprietary Quality Control algorithm to check quality and consistency in patient assessments

• Confirmation of the diagnosis and inclusion/exclusion criteria by central experts

• Standardize patient assessment processes

• Reminders to increase medication adherence and study follow-up

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Assignee: SYNEURX INTERNATIONAL CORP. (Taipei, TW)

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Estimated worldwide human allele frequencies of ApoE * in Caucasian population[57]

Allele ---------------- £`2 ---- £`3 ---- £`4

General Frequency ----- 8.4% -- 77.9% - 13.7%

AD Frequency ---------- 3.9% -- 59.4% - 36.7%

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Åý§Ú­Ì¦b½Æ²ß¤@¤U ( From Wikipedia, the free encyclopedia )

Crenezumab¬O¤@ºØ°w¹ï¤H1-40©M1-42£] ¾ý¯»¼Ë³J¥Õªº§¹¥þ¤H·½¤Æ³æ§J¶©§ÜÅé¡A¥¿¦b¬ã¨s¨ä§@¬°ªüº¸¯ý®üÀq¯fªºªvÀø¤èªk¡C[1] Crenezumab»Psolanezumab°ª«×¦P·½¡Asolanezumab¬O¥t¤@ºØ¹v¦V¾ý¯»¼Ë³J¥Õ-£]肽ªº³æ§J¶©§ÜÅé¡C

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1. CrenezumabªvÀø»P¸£¯á²G¤¤£]-¾ý¯»¼Ë³J¥Õ½è¡]Abeta¡^§C»EÅé¤ô¥­ªº«ùÄò¤U­°¬ÛÃöÁp¡C

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Crenezumab¬OAC Immune¤½¥q§Q¥Î¨äSupraAntigen TM§Þ³N¥­¥xµo²{ªº¤@ºØ§Ü£]-¾ý¯»¼Ë³J¥Õ§ÜÅé¡A¨Ã©ó2006¦~³Q§@¬°ªüº¸¯ý®üÀq¯fªº¤@ºØ¼ç¦bªvÀø¤â¬q¦Ó³\¥iµ¹°ò¦]®õ§J¤½¥q¡CCrenezumab¬O¤@ºØ§¹¥þ¤H·½ªºIgG 4³æ§J¶©§ÜÅé¡A¥¦µ²¦X¤F©Ò¦³§Î¦¡ªº¿ù§éÅ|Abeta³J¥Õ¡A¯S§O¬OAbeta§C»EÅé¡A¥H¨¾¤î©M¯}ÃaAbeta»E¶°¡A«P¶iAbeta¸Ñ»E¡CIgG4¨ÈÃþ¨ã¦³´î¤Öªº®ÄÀ³¾¹¥\¯à¡A¤¹³\¤p½¦½è²Ó­M±q¸£¤¤²M°£Abeta¡A¦P®É³Ì¤p¤Æª¢¯g¤ÏÀ³¡C¡]·s®öÂåÃĽsĶ/David¡^

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Crenezumab ( From Wikipedia, the free encyclopedia )

en.wikipedia.org/wiki/Crenezumab

Clinical trials :

ABBY study

ABBY was a phase II study that evaluated the effects of crenezumab in patients with mild-to-moderate Alzheimer¡¦s Disease, which concluded in 2014. The primary endpoints were reduction in cognitive decline and global function decline.[13] Patients treated with high-dose intravenous crenuzumab showed non-significant reductions in both cognitive decline and global function decline, while patients who received subcutaneous crenezumab did not improve on either measure. Exploratory analysis of patients with the mildest symptoms (as defined by a Mini Mental State Examination score of 22-26) who received high-dose intravenous crenezumab did show a significant reduction in cognitive decline, but not in global function decline.[13]

BLAZE study

BLAZE was a phase II study that also concluded in 2014 and evaluated the effects of crenezumab in patients with mild-to-moderate Alzheimer¡¦s Disease, however its primary endpoint was changes in brain amyloid load, with secondary endpoints of changes in other biomarkers, cognition, global function, and activities of daily living. The resultant data showed no significant difference between either high-dose intravenous or subcutaneous crenezumab and placebo.[13]

CREAD study

In July 2015, Genentech announced it was moving crenezumab into a phase III study, known as CREAD, to evaluate the effects of crenezumab in patients with prodromal-to-mild Alzheimer¡¦s Disease. This study aims to enroll 750 individuals between the ages of 50 and 85 at 233 international sites.[16] The primary outcome measure for this trial is change in clinical dementia rating, with secondary outcomes of changes in cognition, quality of life, and time to clinically evident decline, among others. The study is expected to conclude in 2021.[17]

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W199. Discovery of Novel Inhibitors of D-Amino Acid Oxidase

Guochuan Tsai*

University of California at Los Angeles, Torrance, California, United States

Background: The legendary biochemist, Sir Hans Adolf Krebs discovered D-amino acid deaminase. D-amino acid oxidase (DAAO) is the first enzyme being crystalized. Its main substrate, D-serine and D-alanine are critically important co-agonist of the N-methyl-D-aspartate receptor (NMDAR). We recently demonstrated that sodium benzoate, as a competitive antagonist of DAAO, can substantially improve the positive and negative symptoms and neurocognition of schizophrenia, presumably enhance NMDA function by raising D-serine and D-alanine levels. Also, in mild dementia, sodium benzoate improves the cognition and function.

The development of glutamatergic NMDA treatments in the past two to three decades, is following a similar path of the development of aminergic and GABAergic treatments. All three lines of treatments involve neurotransmitter analogue and its precursor (e.x. chloroziapoxide, tryptophan), agonist/antagonist (L-dopa, chlopromazine), uptake blocker (imipramine, fluoxetine, bupropion), as well as catabolism inhibitor (iproniazid, selegiline). In analogy to the aminergic and GABAergic treatments, the initial discovery was the therapeutic application of the co-agonists/partial agonists, including glycine, D-serine, D-cycloserine and D-alanine. The NMDA treatment options coming up later were obvious in the hindsight; first, the neurotransmitter uptake inhibition by glycine transporter-1 inhibitor; second, NMDAR antagonists; third, the inhibition of the DAAO. The treatment approach of DAAO inhibition is analogous to monoamin oxidase inhibitors (MAOI), which upregulates monoamine for CNS disorders like depression and Parkinson disease. In another word, DAAO inhibitors are similar to MAOI in raising the tone of neurotransmitter of interest, by inhibiting the catabolism enzyme.

Methods: Following the initial success of DAAO inhibition by sodium benzoate, we search for candidate drugs that can safely activate NMDAR, we had screened and identified several DAAO inhibitors that can be potential therapeutics for CNS disorders. For DAAO activity assay, recombinant DAO-6Histidines (400 nM) was added into 3% (w/v) o-phenylenediamine, 1 U horseradish peroxidase, 40 mM D-alanine with a final volume of 200 £gL. The reaction at 25 ¢XC generated hydrogen peroxide that was oxidized by the peroxidase and further converted, in the presence of o-phenylenediamine, to 2,3-diaminophenazine, which was quantified by measuring OD450. For the inhibitor assay, candidate drugs at mM-nM was applied to determine the IC50. To confirm the findings of the enzyme assay, we also perform molecular docking study of the potential DAAO inhibitors. To decide the candidate for new drug development, we test the compounds with low IC50, which were confirmed by docking study, by a battery of animal behavior studies relevant to CNS disorders.

Results: We had identified more than 20 candidate DAAO inhibitors. One of the DAAO inhibitors, SND51, botanic in origin, was confirmed to be a competitive antagonist of DAAO, with IC50 at 5 £gM, which is more potent than sodium benzoate (IC50=61£gM). Repeated administration in rodent does not affect its body weight, food intake, liver and kidney weights, nor gross and histopathology. The findings in carcinogenesis, mutagenesis studies are benign. Its safety profile is satisfactory, with LD50 >1500 mg/Kg in most toxicology studies.

In rodent behavior models, 20 mg/kg administration of SND51 improves spatial memory. It attenuates the MK-801-induced hyperlocomotion and restores sensorimotor gating disrupted by MK-801. It also improve the anxiety performance on elevated plus maze.

Conclusions: Given its activities in bo

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SyneuRx ¤½¥qªñ¨Ó¤G¤T¨Æ

Uspto Issues Trademark: Syneurx

www.highbeam.com/doc/1P4-2020372070.html

The trademark SYNEURX (Reg. No. 5419038) was issued on March 6 by the USPTO.

*****************************

SyneuRx Neuroscience HK Limited (CR No. 2684857)

www.hkcompanycheck.com/syneurx-neuroscience-hk-limited-clxcfee/

SyneuRx Neuroscience HK Limited was incorporated on 23 Apr 2018 as a Private company limited by shares registered in Hong Kong.

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Author(s): Guochuan Emil Tsai.

Journal Name: Current Pharmaceutical Design

Volume 20 , Issue 32 , 2014

DOI : 10.2174/1381612820666140204121732

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Molecular Targets of Tannic Acid in Alzheimer¡¦s Disease.

www.ncbi.nlm.nih.gov/pubmed/28176625

Abstract

Tannic acid (TA)has strong antioxidant/free radical scavenging, antiinflammatory, anti-viral/bacterial, and anti-carcinogenic properties.

TA¨ã¦³±j§Ü®ñ¤Æ¾¯/¦Û¥Ñ°ò²M°£¡A§Üª¢¡A§Ü¯f¬r/²Óµß©M§Ü­PÀù©Ê

The neuroprotective effects of TA against AD have been shown in several in vitro and in vivo models of AD.

Apart from its potent antioxidant and anti-inflammatory roles, evidence suggests that TA is also a natural inhibitor of £]-secretase (BACE1) activity and protein expression.

BACE1 is the primary enzyme responsible for the production and deposition of A£] peptide.

TA also destabilises neurotoxic amyloid beta (A£]) fibrils in vitro.

Apart from its effects on the A£] cascade, TA can also inhibit the in vitro aggregation of tau peptide, a core component of intracellular neurofibrillary tangles (NFTs).

This review summarizes the relevance of TA and TA-related vegetable extracts (tannins) in the pathogenesis of AD and its enzymatic targets.

It also highlights the significance of TA as an important lead compound against AD.

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BIT¡¦s 16th Annual Congress of International Drug Discovery Science and Technology-2018

Theme: Rethinking the Next Big Things in Pharma Innovations

Time: August 16-19, 2018

Place: Boston Marriott Cambridge, USA

www.iddst.com/iddst2018/ScientificProgram3_5.asp

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Session 3704: CNS and Neurodegenerative Disorders Drugs and Therapies

Day 3: Afternoon, Saturday, August 18, 2018

13:30-16:20

Chair: Dr. Guochuan E Tsai, CEO, SyneuRx Neuroscience; Professor-in-Residence, David Geffen School of Medicine, University of California at Los Angeles, USA

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14:00-14:25

Title:

Facilitating NMDA System Balance to Address CNS Disorders

Dr. Guochuan E Tsai, CEO, SyneuRx Neuroscience; Professor-in-Residence, David Geffen School of Medicine, University of California at Los Angeles, USA

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