A Randomized, Double-Blind, Placebo-Controlled Study to Assess the Efficacy and Safety of NYX-2925 in Subjects With Neuropathic Pain Associated With Diabetic Peripheral Neuropathy

To evaluate the efficacy of NYX-2925 versus placebo in treating the neuropathic pain associated with diabetic peripheral neuropathy.

开始日期2019-11-12

申办/合作机构

Aptinyx, Inc.

[+1]

NCT04147858 / Completed临床2期

A Randomized, Double-Blind, Placebo-Controlled Study to Assess the Efficacy and Safety of NYX-2925 in Subjects With Fibromyalgia

To evaluate the efficacy of NYX-2925 versus placebo for the treatment of fibromyalgia.

开始日期2019-11-12

申办/合作机构

Aptinyx, Inc.

[+1]

NCT03249103 / Completed临床2期

A Phase 2, Single-Blind, Exploratory, Placebo-controlled, Pilot Study to Assess the Efficacy and Safety of Daily Oral NYX-2925 in Subjects With Fibromyalgia

The primary objective is to determine whether daily dosing with NYX-2925 changes markers of central pain processing in subjects with fibromyalgia by evaluating changes in evoked pain, and visual stimulation, functional magnetic resonance imaging (fMRI), resting state function connectivity magnetic resonance imaging (rs-fcMRI) and proton magnetic resonance spectroscopy (H-MRS) in fibromyalgia subjects on active drug versus placebo.

开始日期2017-08-14

申办/合作机构

Aptinyx, Inc.

[+1]

100 项与 NYX-2925 相关的临床结果

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100 项与 NYX-2925 相关的转化医学

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100 项与 NYX-2925 相关的专利（医药）

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项与 NYX-2925 相关的文献（医药）

2020-03-01·Journal of neurochemistry2区 · 医学

NYX‐2925 induces metabotropic N‐methyl‐d‐aspartate receptor (NMDAR) signaling that enhances synaptic NMDAR and α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepropionic acid receptor

2区 · 医学

Article

作者: Cacheaux, Luisa P. ; Sennello, Joseph A. ; Khan, M. Amin ; Schmidt, Mary E. ; Sahu, Srishti U. ; Bowers, M. Scott ; Leaderbrand, Katherine ; Moskal, Joseph R. ; Kroes, Roger A.

Abstract:

N‐methyl‐d‐aspartate receptors (NMDARs) mediate both physiological and pathophysiological processes, although selective ligands lack broad clinical utility. NMDARs are composed of multiple subunits, but N‐methyl‐d‐aspartate receptor subunit 2 (GluN2) is predominately responsible for functional heterogeneity. Specifically, the GluN2A‐ and GluN2B‐containing subtypes are enriched in adult hippocampus and cortex and impact neuronal communication via dynamic trafficking into and out of the synapse. We sought to understand if ((2S, 3R)‐3‐hydroxy‐2‐((R)‐5‐isobutyryl‐1‐oxo‐2,5‐diazaspiro[3,4]octan‐2‐yl) butanamide (NYX‐2925), a novel NMDAR modulator, alters synaptic levels of GluN2A‐ or GluN2B‐containing NMDARs. Low‐picomolar NYX‐2925 increased GluN2B colocalization with the excitatory post‐synaptic marker post‐synaptic density protein 95 (PSD‐95) in rat primary hippocampal neurons within 30 min. Twenty‐four hours following oral administration, 1 mg/kg NYX‐2925 increased GluN2B in PSD‐95‐associated complexes ex vivo, and low‐picomolar NYX‐2925 regulated numerous trafficking pathways in vitro. Because the NYX‐2925 concentration that increases synaptic GluN2B was markedly below that which enhances long‐term potentiation (mid‐nanomolar), we sought to elucidate the basis of this effect. Although NMDAR‐dependent, NYX‐2925‐mediated colocalization of GluN2B with PSD‐95 occurred independent of ion flux, as colocalization increased in the presence of either the NMDAR channel blocker (5R,10S)‐(–)‐5‐Methyl‐10,11‐dihydro‐5H‐dibenzo[a,d]cyclohepten‐5,10‐imine hydrogen maleate or glycine site antagonist 7‐chlorokynurenic acid. Moreover, while mid‐nanomolar NYX‐2925 concentrations, which do not increase synaptic GluN2B, enhanced calcium transients, functional plasticity was only enhanced by picomolar NYX‐2925. Thus, NYX‐2925 concentrations that increase synaptic GluN2B facilitated the chemical long‐term potentiation induced insertion of synaptic α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepropionic acid receptor GluA1 subunit levels. Basal (unstimulated by chemical long‐term potentiation) levels of synaptic GluA1 were only increased by mid‐nanomolar NYX‐2925. These data suggest that NYX‐2925 facilitates homeostatic plasticity by initially increasing synaptic GluN2B via metabotropic‐like NMDAR signaling.imageCover Image for this issue: doi: 10.1111/jnc.14735.

2020-01-01·Neurobiology of pain (Cambridge, Mass.)

The NMDAR modulator NYX-2925 alleviates neuropathic pain via a Src-dependent mechanism in the mPFC

Article

作者: Bowers, M Scott ; Ghoreishi-Haack, Nayereh ; Barth, Amanda L ; Moskal, Joseph R ; Morrison, Gladys ; Cearley, Cassia N ; Asiedu, Marina N ; Dunning, Jacqueline ; Priebe, Jessica M ; Kroes, Roger A

Previous studies have shown that oral administration of the NMDAR modulator NYX-2925 alleviates pain in several animal models of neuropathic pain and this appears to be through mPFC, but not spinal, mediated mechanisms. While much is known about the impact of neuropathic pain on NMDAR-mediated signaling in the spinal cord, limited studies have focused on the brain. In the current study, we assess signaling changes associated with NMDAR-mediated plasticity in the mPFC and the impact of NYX-2925 administration on the normalization of these signaling changes. We found a decrease in activated Src levels in the mPFC of animals with chronic constriction injury (CCI) of the sciatic nerve. While Src mediated activation of NMDARs was also decreased in CCI animals, the main NMDAR phosphorylation site of CAMKII was not affected. This is in opposition to what has been found in the spinal cord, where both Src and CAMKII activation are increased. Oral administration of NYX-2925 restored levels of activated Src and Src phosphorylation sites on GluN2A and GluN2B in the mPFC, with no effect on activated CAMKII levels. The analgesic effect of NYX-2925 appears dependent on this restoration of Src activation in the mPFC, as co-administering Src activation inhibitors prevented the NYX-2925 analgesic effect. Overall, these data suggest that NMDAR-mediated signaling plays a key role in neuropathic pain, albeit in different directions in the spinal cord vs. the mPFC. Furthermore, the analgesic effect of NYX-2925 appears to involve a restoration of NMDAR-mediated signaling in the mPFC.

2019-12-01·Psychopharmacology3区 · 医学

A translational EEG-based approach to assess modulation of long-lasting NMDAR-dependent synaptic plasticity

3区 · 医学

Article

作者: Leaderbrand, K ; Madsen, T M ; Sørensen, L ; Christian, E P ; Burgdorf, Jeffrey S ; Moskal, J R ; Khan, M A ; Kroes, R A ; Stanton, P K

BACKGROUND:

NYX-2925 is a novel N-methyl-D-aspartate receptor (NMDAR) modulator that has been shown to facilitate both NMDAR-dependent long-term potentiation (LTP) in vitro and learning and memory in vivo.

OBJECTIVE:

The present studies examine the effects of NYX-2925 on NMDAR-dependent auditory LTP (aLTP) in vivo.

METHODS:

NMDAR-dependent aLTP and NMDAR-dependent auditory mismatch negativity (MMN) was measured, as well as changes in resting-state qEEG power.

RESULTS:

NYX-2925 (1, 10 mg/kg PO) increased aLTP 1 h after auditory tetanus measured by the post- minus pre-tetanus difference waveform 140-180 ms post tone onset. NYX-2925 (0.1, 1 mg/kg PO) facilitated MMN measured by the difference waveform (i.e., deviant minus standard tones). NYX-2925 (0.1, 1, 10 mg/kg PO) also enhanced resting-state alpha qEEG power. Conversely, the NMDAR glutamate site antagonist CPP (10 mg/kg IP) reduces alpha power and MMN and produces an opposite effect as NYX-2925 on aLTP.

CONCLUSIONS:

Together, these data suggest that the activation of the NMDAR by NYX-2925 enhances synaptic plasticity in vivo, which may both reduce symptoms of neurological disorders and serve as a biomarker for drug effects. This is the first demonstration of a long-lasting (1-h post-tetanus) effect of NMDAR modulation on synaptic plasticity processes in vivo using a noninvasive technique in freely behaving animals.

项与 NYX-2925 相关的新闻（医药）

2023-03-01

·药时代

3个临床试验全部输给安慰剂，是天灾还是人祸？

创新药BD高阶研讨会【上海站】！点击这里立刻报名！撰文| 菜一碟有这么一家Biotech，8年时间，只做一个靶点。基于这个靶点，这家Biotech铺出了3条管线，共4个适应症，还将这4个适应症都带到了2期临床，4个适应症分别为：糖尿病周围神经性疼痛(DPN)、纤维肌痛综合征(FM)、帕金森氏病认知障碍(PDD)、创伤后应激障碍(PTSD)。（都是CNS的天坑）可惜，如今这3条管线全部“扑街”（失败*2，自愿停止*1），除了关于PTSD的2期试验是自愿停止外，其他2期试验均败给了安慰剂。他就是Aptinyx（以下简称A司），一家专注于发现和开发治疗大脑和神经系统疾病的创新疗法的Biotech。A司的独到之处在于，他的所有候选产品都是NMDA受体调节剂。NMDA受体（N-甲基-D-天冬氨酸受体）是中枢神经系统发育的重要组成部分，其作用是控制突触可塑性，介导学习和记忆功能。如果NMDA受体被过度激活，会导致Ca2+过量流入神经元，引起细胞死亡，这种现象被称为兴奋毒性，而兴奋毒性又与神经退行性病变（中风、帕金森、老年痴呆等）有关。反之，当NMDA受体被阻断时，会改变突触间的信号传递，导致幻听、认知障碍、精神分裂等。那么理论上，只要合理控制NMDA受体的活性，便可治疗由此（NMDA受体过度激活/阻断）引发的一系列疾病。而A司的NMDA受体调节剂，是有选择性地激活某些亚型的NMDA受体的能力，而不是直接过度激活或阻断NMDA受体。减少其副作用，从而达到更温和的效果、更好的安全性和耐受性。既然理论上非常可行，又为何做起试验“一碰就碎”（干不过安慰剂）?先看试验。A司共有NYX-2925、NX783、NX458三条管线，以NYX-2925为例（A司最重要也最早的管线），NYX-2925做了两个适应症：糖尿病周围神经性疼痛(DPN)、纤维肌痛综合征(FM)。2016年，NYX-2925完成1期临床试验入组（入组人数84），同年获FDA授予的快速通道指定，2017年试验完成，结果积极。NYX-2925的1期试验是一项随机、双盲、安慰剂对照的剂量递增试验，旨在评估NYX-2925在健康志愿者中的安全性、耐受性和药代动力学。该试验共招募了84名志愿者，分为单次口服组和多次口服组，分别给予不同剂量的NYX-2925或安慰剂。1期结果显示，NYX-2925在所有剂量水平下均表现出良好的安全性和耐受性，没有出现严重不良事件或停药事件。NYX-2925还显示出与预期相符的药代动力学特征，具有快速吸收、高生物利用度和适中的半衰期。基于此项结果，A司快速推进NYX-2925(DPN)的2a试验。NYX-2925（DPN）的2a试验是一项随机、双盲、安慰剂对照、多中心的临床试验，共招募了300名DPN患者，分别给予10mg、50mg或200mg NYX-2925或安慰剂，每天一次，连续28天。2a试验的主要终点是评估NYX-2925对改善11点数值评分量表(NRS)上的平均每日最低疼痛强度 (ADLPI)的效果。2a试验结果显示，在总体患者群中，NYX-2925在50 mg剂量组达到了统计学和临床上显著改善ADLPI的效果，而10mg和200mg剂量组则未达到显著差异。A司在官方新闻稿里重点强调了，在DPN较重的患者群中(基线时NRS评分27)，NYX-2925在50 mg剂量组表现出更强的止痛效果，而其他两个剂量组也显示出趋势性改善此外，试验还发现NYX-2925具有良好的药代动力学特征和耐受性。这个结果看上去没什么毛病，50mg效果显著，唯一的缺陷就是没做出剂量相关性，但正是这个小缺陷暗示了后续所有临床试验的失败，具体请看全人群的临床数据。在全人群的疗效结果里，不仅没有做出剂量相关性，10mg剂量组的疗效还要弱于安慰剂。不过A司并没有把这个数据放在心上，在NYX-2925（DPN）的2a试验之后，便就50mg的剂量做了2b试验。NYX-2925（DPN）的2b试验主要针对晚期疼痛性DPN患者的一项随机、双盲、安慰剂对照的临床试验，共招募了229名患者，分别给予50 mg NYX-2925或安慰剂，每天一次，连续28天。2b试验的主要终点是评估NYX-2925对改善NRS上的ADLPI的效果。2b试验结果显示，在总体患者群中，NYX-2925末能达到主要终点(与安慰剂相比差异为0.24分;p=0.54)，也未能在任何次要终点上显示出显著改善。头铁的娃又去做了NYX-2925（纤维肌痛综合征），结果不出意外，惨遭失败。同样的事情还发生在NYX-458(帕金森适应症)的2期试验上。这样的失败到底是天灾还是人祸？如今（2022年2月27日），A司宣布要削减成本，寻找替代方案，主动暂停了还没出结果的NYX-783（PTSD）。也就是说，A司已经没有“回天”的机会了。至于管线中的NYX-783（阿片类药物使用障碍、OUD）仍处IND阶段，连同管线的2期都停了，不停它完全是因为A司没法停。2022年，美国国立卫生研究院（NIH）拨款560万美元，资助A司用于NYX-783（OUD）的开发。根据A司最新财报（2022年第三季度）：截至2022年9月30日，现金和现金等价物为6650万美元，2022年初还有1.061亿美元，3个月内研发费用为1000万美元。当时，A司预计还能撑到2024年，现在看来由于2023年2月NYX-783的失败，A司要提前收场了。再看二级市场，NYX-2925（DPN）的2a试验结果出来后，A司股价出现大跳水，从最高点30美元跳到5美元。后来A司又2次增发股票，让自己的股价再无波澜，一片坦途。如今A司股价不到0.2美元，总市值从9.7亿美元缩水至1327亿美元。A司在官网上的第一篇新闻稿中这样写道：“当我们结束Naurex（Naurex被收购后，A司从中剥离出来）故事的最后一章时，我们很高兴与Aptinyx重新开始......”8年过去，投资人和他们应该都不是很高兴。参考资料：1.Aptinyx官网2.FDA官网3.https://clinicaltrials.gov/ct2/results?cond=NYX-2925&draw=2&rank=4#rowId34.其他公开资料封面图来源：电影《破坏之王》推荐阅读3期疗效还没出，光有药代动力学结果，股价就大涨70%……辉瑞要收购Seagen？华尔街日报：正在谈判！问了CHATGPT亲兄弟「中国药企会面临哪些风险」虽然是车轱辘话，但好像很有道理……点击这里，报名创新药BD高阶研讨会【上海站】！

临床2期快速通道临床1期

2023-02-28

·MedCity News

Parkinson’s Trial Failure Signals a Likely End for CNS Biotech Aptinyx

Aptinyx’s approach of treating neurological disorders by targeting a key receptor in the brain has fallen short again, this time in Parkinson’s disease. With its third clinical trial failure in less than a year, the biotech said it will end the Parkinson’s program as well as a separate one in post-traumatic stress disorder. The drug candidate for Parkinson’s, NYX-458, was in testing as a potential treatment for mild cognitive impairment or mild dementia associated with that disease or a closely related neurological disorder called dementia with Lewy bodies. The once-daily pill was being evaluated in a 99-patient, placebo-controlled study. According to preliminary results released after Monday’s market close, the Aptinyx drug did not show clinically meaningful improvement as assessed using tests to evaluate function and cognition in Parkinson’s patients. “The results overall do not support further advancement of the development program by Aptinyx,” the company said in its announcement. Evanston, Illinois-based Aptinyx develops small molecule drugs that target and modulate N-methyl-D-asparate (NMDA) receptors. These receptors are important to normal function of the brain and central nervous system. Aptinyx’s drugs stem from its platform technology for discovering molecules that can modulate NMDA receptors. The Aptinyx technology has yielded drug candidates for chronic pain, Parkinson’s, and PTSD. Last April, Aptinyx reported that chronic pain drug NYX-2925 failed to distance itself from a placebo in a Phase 2 study enrolling patients with diabetic peripheral neuropathy. The company continued a mid-stage test assessing the drug in fibromyalgia. Last August, the chronic pain drug failed that study as well. After the Parkinson’s failure, Aptinyx isn’t waiting to see the results for drug candidate NYX-783 in PTSD. The company said it will terminate that study and analyze the data to determine its next steps for that program. Aptinyx also said it will implement cost-cutting measures and explore “strategic alternatives,” which could mean a sale of the company or its assets, or perhaps a merger with a privately held biotech looking for way to enter the public markets. Aptinyx’s drug discovery technology came from Naurex, a psychiatric drugmaker that was acquired by Allergan in 2015. That year, Aptinyx launched to develop its NMDA receptor-targeting drugs. The company went public in 2018, pricing its shares at $16 each and raising nearly $118 million. Shares of Aptinyx opened Tuesday at 20 cents apiece. Image: Dr_Microbe, Getty Images

临床2期

2023-02-28

·FierceBiotech

Aptinyx, reeling from series of setbacks, dumps dementia drug, stops PTSD trial after phase 2 flop

Aptinyx is yet to publicly disclose layoffs but said it will “undertake cost-cutting measures.” Serial clinical trial train wreck Aptinyx is at it again. After seeing a pain prospect flunk three clinical trials, the biotech has added Parkinson's disease and dementia to its list of failed indications—prompting it to stop work on its two clinical candidates, cut costs and seek strategic alternatives. Last year, the third midphase failure of NYX-2925 prompted Aptinyx to drop the pain program and switch its attention to a pair of other NMDA receptor positive allosteric modulators, NYX-458 and NYX-783. The delivery of data from a phase 2 clinical trial of NYX-458 has prompted the company to rethink its plans once again and sent its stock down 54% to 27 cents in premarket trading. The midphase study randomized 99 patients with mild cognitive impairment or mild dementia caused by Parkinson’s or Lewy body dementia to receive NYX-458 or placebo for 12 weeks. Aptinyx began the trial on the basis of evidence that the molecule boosts cognition by addressing glutamatergic dysregulation. Across a slate of efficacy endpoints, NYX-458 failed to deliver on the preclinical promise. Aptinyx is yet to share data from the trial but revealed the absence of clinically meaningful improvements. The efficacy endpoints included two evaluations of the patients’ everyday functions and a battery of computerized neurocognitive tests designed to assess cognition. The comprehensive failure led Aptinyx to drop plans for further development of NYX-458. The fallout has hit the rest of the business, with the biotech terminating an ongoing study of NYX-783 in post-traumatic stress disorder (PTSD) early. Aptinyx had expected to report phase 2b data in PTSD in the second half of the year. Now, the biotech will review the data generated on NYX-783 to date to inform the next steps while trying to conserve its cash and identify a way out of its current predicament. Aptinyx is yet to publicly disclose layoffs but said it will “undertake cost-cutting measures.” The biotech ended September with $67 million to its name.

临床2期

100 项与 NYX-2925 相关的药物交易

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适应症	最高研发状态	国家/地区	公司	日期
糖尿病周围神经性疼痛	临床2期	美国	Aptinyx, Inc.	2019-11-12
纤维肌痛	临床2期	美国	Aptinyx, Inc.	2017-08-14
糖尿病周围神经病变	临床2期	美国	Aptinyx, Inc.	2017-06-27

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适应症

分期

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研究	分期	人群特征	评价人数	分组	结果	评价	发布日期


NCT04147858 (CTgov)	临床2期	纤维肌痛	310	NYX-2925 (NYX-2925 50 mg)	夢廠齋築醖網鏇鹹廠鏇(鹹築淵糧構餘壓遞窪壓) = 鏇願齋廠衊鹹顧憲簾壓構構淵鹽網憲製範鹹網 (鹽夢簾廠獵膚鑰鹽艱襯, 願廠製淵觸齋鑰觸鬱衊 ~ 選選糧鬱網範鹹選蓋醖) 更多	-	2023-04-28
				NYX-2925 (NYX-2925 100 mg)	夢廠齋築醖網鏇鹹廠鏇(鹹築淵糧構餘壓遞窪壓) = 顧糧選鹽醖獵選衊獵窪構構淵鹽網憲製範鹹網 (鹽夢簾廠獵膚鑰鹽艱襯, 範構衊構製壓襯顧鹹糧 ~ 鑰顧構壓艱壓廠壓膚窪) 更多
NCT04146896 (CTgov)	临床2期	糖尿病周围神经病变 \| 糖尿病周围神经性疼痛	228	NYX-2925 50 mg (NYX-2925)	醖製遞顧壓蓋獵淵窪餘(餘餘廠鏇鏇築願衊網鏇) = 淵簾構獵遞廠憲鹽襯齋醖鬱鑰艱糧鏇醖選觸鹹 (顧淵網遞觸鑰鏇艱鬱積, 築糧鏇鹹鹽鹽顧淵衊齋 ~ 顧齋鑰簾蓋衊壓壓觸構) 更多	-	2023-04-28
				Placebo (Placebo)	醖製遞顧壓蓋獵淵窪餘(餘餘廠鏇鏇築願衊網鏇) = 夢鏇糧窪網衊壓鑰構顧醖鬱鑰艱糧鏇醖選觸鹹 (顧淵網遞觸鑰鏇艱鬱積, 淵蓋淵淵餘窪獵壓窪醖 ~ 積醖積獵鬱淵淵網鑰築) 更多
NCT03249103 (CTgov)	临床2期	纤维肌痛	22	Placebo+NYX-2925	憲襯廠窪網積鏇構蓋繭(艱蓋齋觸製艱醖選醖觸) = 艱廠簾窪鹽積壓壓鹽積膚壓鑰餘鹽願遞廠齋鏇 (醖遞窪醖構鏇構醖蓋簾, 蓋範艱鏇艱壓窪夢膚遞 ~ 觸築遞襯憲網鏇鹽遞壓) 更多	-	2022-09-16
NCT04147858 (BusinessWire) 人工标引	临床2期	纤维肌痛	300	NYX-2925	蓋蓋網餘淵餘襯簾鏇獵(鑰襯衊衊艱壓憲構積鏇) = NYX-2925 did not achieve the primary endpoint of the study 蓋網遞襯艱築構鑰鬱築 (築構選網獵窪膚築淵遞 )	不佳	2022-08-12
				Placebo
NCT03219320 (CTgov)	临床2期	神经痛 \| 糖尿病周围神经病变	301	NYX-2925 (NYX-2925 200 mg QD)	鏇艱糧艱窪鏇廠簾襯遞(製鏇製鑰膚觸壓衊築獵) = 憲窪鏇艱淵網網鑰鬱鬱窪簾膚齋廠觸築網獵獵 (壓築簾顧積窪製蓋積衊, 膚餘壓憲夢選淵齋顧簾 ~ 艱構鏇憲鹽鑰襯齋糧蓋) 更多	-	2020-06-09
				NYX-2025 (NYX-2025 50 mg QD)	鏇艱糧艱窪鏇廠簾襯遞(製鏇製鑰膚觸壓衊築獵) = 襯襯蓋鹹獵餘窪網襯網窪簾膚齋廠觸築網獵獵 (壓築簾顧積窪製蓋積衊, 壓鏇艱顧襯襯艱網範鑰 ~ 憲築衊廠糧蓋襯鏇鹽艱) 更多
NCT03249103 (GlobeNewswire) 人工标引	临床2期	纤维肌痛	23	NYX-2925	積齋積窪齋簾襯蓋觸獵(鬱膚衊醖鏇觸襯獵鑰築) = 獵齋獵築襯艱築淵構衊窪襯簾鹹衊選選齋醖獵 (範願齋齋鹹積繭獵範積 ) 更多	积极	2019-06-10
				Placebo	積齋積窪齋簾襯蓋觸獵(鬱膚衊醖鏇觸襯獵鑰築) = 構顧廠鏇醖顧選衊壓獵窪襯簾鹹衊選選齋醖獵 (範願齋齋鹹積繭獵範積 ) 更多
NCT03219320 (GlobeNewswire) 人工标引	临床2期	糖尿病周围神经病变	300	NYX-2925	醖鬱鹽齋觸艱蓋鏇糧憲(蓋鹹選簾鏇簾窪衊艱廠) = 餘憲艱膚築糧糧襯襯齋選壓淵壓淵鑰艱衊衊獵 (鏇遞憲襯鏇蓋夢繭觸餘 )	不佳	2019-01-16
				Placebo	醖鬱鹽齋觸艱蓋鏇糧憲(蓋鹹選簾鏇簾窪衊艱廠) = 鹽艱鏇夢鬱鏇顧築蓋構選壓淵壓淵鑰艱衊衊獵 (鏇遞憲襯鏇蓋夢繭觸餘 )