预约演示

更新于：2025-07-19

Oxycodone

羟考酮

更新于：2025-07-19

概要

基本信息

简介Oxycodone是一种阿片类止痛药物，有时也被称为麻醉剂。它是一种通过结合大脑和脊髓中的μ、κ和δ受体来缓解疼痛的阿片类药物。Oxycodone的化学名称为4,5 α-环氧-14-羟基-3-甲氧基-17-甲基吗啡酮-6-酮。该药物在美国和中国获得批准，并由Collegium制药公司生产。Oxycodone是一种高效的止痛药物，常用于管理中度到重度疼痛，如癌症、手术或创伤引起的疼痛。然而，由于其成瘾和滥用的潜在风险，它被列为受控物质，只能在医疗专业人士的指导下使用。

药物类型

小分子化药

别名

(-)-14-Hydroxydihydrocodeinone、4,5-Epoxy-14-hydroxy-3-methoxy-17-methylmorphinan-6-one、4,5alpha-Epoxy-14-hydroxy-3-methoxy-17-methylmorphinan-6-one

+ [21]

靶点

Opioid receptors

作用方式

激动剂

作用机制

Opioid receptors激动剂(阿片样受体激动剂)

治疗领域

神经系统疾病其他疾病

在研适应症

疼痛术后疼痛急性疼痛

非在研适应症

癌症疼痛慢性疼痛药物滥用+ [3]

原研机构

Collegium Pharmaceutical, Inc.

在研机构

Ensysce Biosciences, Inc.Napp Pharmaceutical Holdings Ltd.

Collegium Pharmaceutical, Inc.

非在研机构

Mundipharma Research GmbH & Co. KG

萌蒂（中国）制药有限公司Grunenthal SA

权益机构

Quotient Sciences Ltd.

Ensysce Biosciences, Inc.

DURECT Corp.

+ [1]

最高研发阶段批准上市

首次获批日期

中国 (2004-01-21),

疼痛

最高研发阶段(中国)批准上市

特殊审评突破性疗法 (美国)、快速通道 (美国)

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结构/序列

分子式C18H21NO4

InChIKeyBRUQQQPBMZOVGD-XFKAJCMBSA-N

CAS号76-42-6

关联

179

项与羟考酮相关的临床试验

NCT06602271

/ Not yet recruiting临床3期

A Multicenter, Randomized, Double-Blind, Placebo- and Active-Controlled Study to Evaluate the Efficacy and Safety of PF614 for the Treatment of Moderate to Severe Pain After Abdominoplasty

The goal of this clinical trial is to evaluate the analgesic activity of PF614 (an oral oxycodone prodrug extended-release analgesic) for control of postsurgical pain in subjects scheduled for abdominoplasty surgery. The main question to be answered is:
• To assess the analgesic efficacy of PF614 compared to oxycodone hydrochloride (an immediate-release opioid analgesic) and placebo in subjects with moderate to severe pain following abdominoplasty Participants will be asked to take oral blinded doses of study medication at about one hour before surgery starts, and then every 6 hours after surgery for up to 4 days.
Participants will be asked to:
* Rate their pain on a 0-10 numerical rating scale (NRS) at various timepoints up to 5 days following surgery;
* Tell us about the need for rescue medication if they continue to have moderate-to-severe pain;
* Tell us about any side effects or adverse effects that they may experience to help us understand the safety and tolerability of the test medications;
* Provide periodic blood samples to help us understand how much study drug is in their system.
Participants will stay in a clinic setting and be monitored for safety for 5 days following surgery. We anticipate that participants will be discharged on Day 5, pending medical review, and then keep a diary to record study-related pain and adverse effects for an additional 2-4 days after discharge.

开始日期2025-03-01

申办/合作机构

Ensysce Biosciences, Inc.

ITMCTR2024000763

/ Suspended临床4期IIT

he Application of Transcutaneous Acupoint Electrical Stimulation Combined with Oxycodone in the Perioperative Period

开始日期2024-12-03

申办/合作机构

徐州市中医院

ChiCTR2400092872

/ Suspended早期临床1期IIT

Observation and Safety Analysis of the Clinical Efficacy of Oxycodone in Preventing Postoperative Delirium in Elderly ICU Patients Undergoing Abdominal Surgery

开始日期2024-12-01

申办/合作机构-

100 项与羟考酮相关的临床结果

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100 项与羟考酮相关的转化医学

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100 项与羟考酮相关的专利（医药）

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7,573

项与羟考酮相关的文献（医药）

2025-12-31·Canadian Journal of Pain-Revue Canadienne de la Douleur

Percutaneous auricular neuromodulation to treat pain after ambulatory breast surgery: A randomized, double-masked, sham-controlled pilot study

Article

作者: Sztain, Jacklynn F. ; Schaar, Adam ; Ilfeld, Brian M. ; Griggs, Jonna L. ; Said, Engy T. ; Abdullah, Baharin ; Abramson, Wendy B. ; Wallace, Anne M. ; Finneran, John J. ; Jensen, Evan J.

Introduction:

Percutaneous auricular neuromodulation involves implanting electrodes around the ear and administering an electric current. A device is currently available that is cleared to treat symptoms from opioid withdrawal, and multiple reports suggest a possible postoperative analgesic effect. This randomized, controlled pilot study aimed to (1) assess the feasibility of a postoperative auricular neuromodulation protocol and (2) provide an estimate of its treatment effects on postoperative pain and opioid consumption.

Methods:

Adults undergoing unilateral or bilateral ambulatory breast surgery with anticipated moderate-severe pain and a single-injection paravertebral nerve block(s) received an auricular neuromodulation device (NSS-2 Bridge, Masimo) following surgery. Participants were randomized to 5 days of electrical stimulation or sham in a double-masked fashion.

Results:

In the first 5 days, the median pain for those receiving active stimulation (n = 15) was 0 (interquartile range [IQR] = 0, 0.5] versus 1.5 (IQR = 0, 3.8) for the sham group (n = 15, P = 0.084). Concurrently, the median oxycodone use for active stimulation was 0 mg (IQR = 0, 2.5) compared to 0 mg (IQR = 0, 3) for the sham group (P = 0.905). Various secondary outcomes reached statistical significance, including maximum and average daily pain scores.

Conclusions:

This pilot study demonstrates that percutaneous auricular neuromodulation is a feasible approach for managing pain in ambulatory surgical procedures and shows potential as an effective analgesic following discharge. Considering its ease of application, absence of systemic side effects, and lack of significant complications, conducting a definitive clinical trial seems justified because the current study was underpowered, which possibly resulted in the lack of statistical significance for the primary outcome.Registry: Clinicaltrials.gov NCT05521516.

2025-12-01·European Journal of Trauma and Emergency Surgery

Pre-injury narcotic drug use in isolated severe traumatic brain injury: effect on outcomes

Article

作者: Demetriades, Demetrios ; Jakob, Dominik Andreas ; Takahashi, Kyosuke ; Yamaguchi, Keishi ; Matsushima, Kazuhide ; Abe, Takeru

PURPOSE:

The aim of this study was to explore the association between pre-injury narcotic drug use (opioids, methadone, and/or oxycodone) and outcomes in isolated severe traumatic brain injury (TBI) patients.

METHODS:

ACS TQIP study included adult trauma patients (≥ 16 years) with complete drug and alcohol screening. Isolated severe TBI was defined as head trauma with AIS 3-5 and without significant extracranial trauma. Exact matching was used to compare patients with isolated pre-injury narcotic drug use to those with no illicit drug or alcohol use. Patients were matched 1:1 based on the following matching criteria: age, gender, mechanism of injury, Injury Severity Score, systolic blood pressure, head AIS, and comorbidities.

RESULTS:

Of 1,846,630 patients, 141,058 had isolated severe head injuries with complete drug and alcohol screenings. After exact matching, 1,560 patients in each group were analyzed. There were no significant differences in hospital mortality, craniectomy rates, complication rates, or length of hospital stay. Patients that tested positive for narcotics had lower rates of mechanical ventilation (16.5% vs. 25.3%, p < 0.01) and shorter ICU stays [3 (2-4) days vs. 3 (2-6) days; p < 0.01].

CONCLUSION:

Pre-injury narcotic drug use in isolated severe TBI is not associates with adverse outcomes. Further research is needed to understand the biochemical and physiological effects of narcotic drugs on TBI outcomes.

2025-11-01·NEUROPHARMACOLOGY

Blocking IL-17A inhibits methamphetamine-induced hyperlocomotion and conditioned place preference and prevents methamphetamine abstinence-induced depression-like behaviors in mice

Article

作者: Koltsova, Ekaterina K ; Szmacinski, Alexandra ; Grivennikov, Sergey ; Meissler, Joseph J ; Wiah, Sonita ; Inan, Saadet ; Dunn, Scott ; Rawls, Scott M

We demonstrated previously that blocking IL-17A, a proinflammatory cytokine, prevents oxycodone-induced depression-like effects and anxiety-like effects during abstinence from MDPV (a psychostimulant) in rats. Here, we tested the hypothesis that eliminating IL-17A signaling (pharmacological antagonism using IL-17A Ab or genetic deletion of IL-17RC) would inhibit behavioral and neurochemical effects elicited by methamphetamine (METH) exposure and abstinence in adult mice. We investigated rewarding and locomotor-activating effects of METH and withdrawal-induced anxiety- and depression-like effects during METH abstinence. Mice received saline or METH (5 mg/kg, IP) once daily for 18 d. Locomotion was measured on days 1 and 15. Anxiety- and depression-like effects were investigated 72 and 96 h after the last METH injection using the elevated plus maze and forced swim test, respectively. IL-17A antibody (Ab, 60 μg/100 μl, IP) was injected every 3rd day of METH exposure. METH-induced hyperlocomotion was significantly reduced in IL-17RC knockout mice or by treatment with the IL-17A Ab (100 μg/100 μl). Neutralization of IL-17A or genetic deletion of IL-17RC prevented development of depression-like effects during METH abstinence. Also, mRNA levels of IL-17RC, but not IL-17RA, in the NAC were enhanced during METH abstinence. Development of METH conditioned place preference (CPP) was prevented by IL-17A Ab but was not affected by IL-17RC deletion in mice conditioned with METH (3 mg/kg) for 4 d. Our data show that abolishing IL-17A signaling reduces METH-induced hyperlocomotion and CPP and attenuates depression-like effects during METH abstinence. These results highlight studying IL-17A blockade as a neuroimmune-based approach to mitigate METH adverse effects.

239

项与羟考酮相关的新闻（医药）

2025-07-16

·ir.ensysce.com

Ensysce Biosciences Initiates Pivotal Phase 3 Study of PF614 - A Next-Generation Opioid - Designed to Deliver Powerful Pain Relief and Reduce Abuse

~ FDA Protocol Review Completed ~ ~ Rho, Inc. Selected as Clinical Research Partner ~ SAN DIEGO, CA / ACCESS Newswire / July 16, 2025 / Ensysce Biosciences, Inc. (NASDAQ:ENSC) ("Ensysce" or the "Company"), a clinical-stage pharmaceutical company pioneering novel solutions for severe pain with built-in abuse and overdose protection, today announced the initiation of its pivotal Phase 3 study of PF614, the Company's lead product candidate. This landmark study, PF614-301, ‘A Multicenter, Randomized, Double-Blind, Placebo- and Active-Controlled Study to Evaluate the Efficacy and Safety of PF614 for the Treatment of Moderate to Severe Pain after Abdominoplasty' is designed to demonstrate PF614's ability to effectively manage post-surgical pain while protecting from abuse and offering patients what is believed to be a safer alternative to conventional opioids. The study aims to confirm that PF614 delivers powerful pain relief and facilitates the transition to non-opioid out-patient care. To execute this critical program, Ensysce has partnered with Rho, Inc., a leading Clinical Research Organization with extensive expertise in central nervous system (CNS) disorders and pain studies. Over the past five years, Rho has successfully managed more than 90 neurology and psychiatry trials at over 840 sites, guiding programs from first-in-human trials to regulatory approval - making them an ideal partner for Ensysce's transformative mission. "In our view, this is more than a partnership. It's a coordinated effort to execute a pivotal study, and a significant step toward redefining pain therapy." said Dr. Lynn Kirkpatrick, CEO of Ensysce. "Our goal is to deliver a new class of opioids that delivers relief from severe pain while protecting patients from the dangers of abuse. We believe PF614 can set a new standard of safety for millions of patients who depend on these medications for a good quality of life." About Ensysce Biosciences Ensysce Biosciences is a clinical-stage pharmaceutical company disrupting the pain treatment landscape with its proprietary Trypsin-Activated Abuse Protection (TAAP™) and Multi-Pill Abuse Resistance (MPAR®) platforms. By engineering opioids with intrinsic safeguards against tampering, misuse, and overdose, Ensysce aims to offer safer, life-saving options for patients in need of powerful pain relief. Learn more at: www.ensysce.com Forward-Looking Statements Statements contained in this press release that are not purely historical may be deemed to be forward-looking statements for the purposes of the safe harbor provisions under The Private Securities Litigation Reform Act of 1995 and other federal securities laws. Without limiting the foregoing, the use of words such as "may," "intends," "can," "might," "will," "expect," "plan," "possible," "believe" and other similar expressions are intended to identify forward-looking statements. The product candidates discussed are in clinic and not approved and there can be no assurance that the clinical programs will be successful in demonstrating safety and/or efficacy, that Ensysce will not encounter problems or delays in clinical development, or that any product candidate will ever receive regulatory approval or be successfully commercialized. All forward-looking statements are based on estimates and assumptions by Ensysce's management that, although Ensysce believes to be reasonable, are inherently uncertain. All forward-looking statements are subject to risks and uncertainties that may cause actual results to differ materially from those that Ensysce expected. In addition, Ensysce's business is subject to additional risks and uncertainties, including among others, the initiation and conduct of preclinical studies and clinical trials; the timing and availability of data from preclinical studies and clinical trials; expectations for regulatory submissions and approvals; potential safety concerns related to, or efficacy of, Ensysce's product candidates; the availability or commercial potential of product candidates; the ability of Ensysce to fund its continued operations, including its planned clinical trials; the dilutive effect of stock issuances from our fundraising; and Ensysce's and its partners' ability to perform under their license, collaboration and manufacturing arrangements. These statements are also subject to a number of material risks and uncertainties that are described in Ensysce's most recent quarterly report on Form 10-Q and current reports on Form 8-K, which are available, free of charge, at the SEC's website at www.sec.gov. Any forward-looking statement speaks only as of the date on which it was made. Ensysce undertakes no obligation to publicly update or revise any forward-looking statement, whether as a result of new information, future events or otherwise, except as required under applicable law. Ensysce Biosciences Company Contact: Lynn Kirkpatrick, Ph.D. Chief Executive Officer (858) 263-4196 Ensysce Biosciences Investor Relations Contact: Shannon Devine MZ North America Main: 203-741-8811 ENSC@mzgroup.us SOURCE: Ensysce Biosciences Inc. Released July 16, 2025

临床3期

2025-07-10

·FiercePharma

State AGs unveil opioid settlements totaling $720M with 8 drugmakers

The eight companies will together pay impacted states and governments up to $720 million, according to announcements from state attorneys general. Eight drugmakers agreed to put legal claims stemming from their roles in the U.S. opioid epidemic to rest with settlements that come out to a combined $720 million, according to Thursday press releases from numerous state attorneys general.Over timeframes ranging from a single year to ten years, Viatris agreed to fork over $284 million, while Amneal committed to $71.7 million in settlement payments and Apotex is on the hook for $63.7 million, according to a release from Pennsylvania's AG. Other companies involved in the settlements are Hikma ($95.8 million), Indivior ($38 million), Sun Pharma ($30.9 million), Alvogen ($18.7 million) and Zydus ($14.8 million).Viatris, which committed the biggest chunk in this group of settlements, previously disclosed a nationwide settlement framework that it hopes will “provide closure on these matters” and resolve opioid-related claims by states, local governments and Tribes against the company and its subsidiaries, the drugmaker said in an April press release. Depending on the level of participation in its settlement, Viatris agreed to pay up to a maximum of $335 million in annual payments over a nine-year period.Some drugmakers will also provide opioid addiction treatment medications under the deals, according to a press release from New York Attorney General Letitia James. Others will provide cash in lieu of those products. In addition, each company—besides Indivior—will be prohibited from marketing products that contain more than 40 mg of oxycodone per pill, according to Pennsylvania's AG. Indivior, for its part, will halt the manufacturing of opioid products for the next ten years but can continue selling treatments for opioid use disorder, according to the deal announcements.The settlements were moved along by “overwhelming participation” from AGs across the country, prompting all eight companies involved to move forward with a “sign-on period” for local governments to participate in the deals. North Carolina, California, Colorado, Illinois, New York, Oregon, Tennessee, Utah and Virginia were responsible for negotiating the deals.“While nothing can compensate for the lives lost and upended by the ongoing opioid crisis, I am grateful to secure these funds on behalf of Massachusetts residents who have been devastated by the crisis —funds that will meaningfully support opioid prevention, harm reduction, recovery, and more,” Massachusetts AG Joy Campbell said in a press release. The settlements are the latest in a wide-ranging web of litigation over the U.S. opioid epidemic. Last month, all 50 U.S. states plus Washington, D.C., and four U.S. territories agreed to sign on to a massive $7.4 billion settlement from Purdue Pharma and the Sackler family, its billionaire founding family.Other than the Sacklers, large opioid-related settlements have come from companies including Teva, Mallinckrodt, Endo and Amneal. In 2022, Johnson & Johnson and three drug distributors inked a landmark $26 billion settlement to resolve more than 3,000 lawsuits.

专利侵权

2025-07-04

·靶点圈

GLP-1RA为何成为代谢领域的 “明星分子”？一文揭秘其传奇诞生之路

01GLP-1/GLP-1R的生物学特性GLP-1的结构与表达调控● GLP-1的来源与结构：主要由肠道L细胞、胰岛α细胞和孤束核神经元分泌，是前胰高血糖素经酶解后产生的肽类激素，与胰高血糖素有约50%的同源性，有GLP-1(7-36)和GLP-1(7-37)两种活性形式。● GLP-1的表达调控①相关受体激活：短链脂肪酸(SCFAs)激活GPR41和GPR43受体、单酰甘油激活GPR119受体、胆汁酸激活GPBA-R受体、鸟苷和尿鸟苷激活鸟苷环化酶(GC-C)受体等，均可促进GLP-1分泌。②肠道菌群结构：菌群失衡会减少SCFAs生成，削弱激活SCFAs受体的能力，影响GLP-1分泌，导致糖脂代谢异常。③天然产物：通过激活苦味受体、GPR-120等靶点，促进GLP-1分泌或增强其信号，可作为GLP-1RAs的替代或辅助治疗，安全性高且副作用少，适合长期管理代谢疾病。表1 对GLP-1具有调节作用的天然产物④饮食因素：高脂饮食会降低肠道产生GLP-1的上皮细胞密度和相关转录因子表达。⑤手术因素：Roux-en-Y胃旁路手术可使人类和动物模型餐后GLP-1浓度显著增加，可能与肠道L细胞数量增加或分泌增加有关。⑥其他因素：钠-葡萄糖协同转运蛋白1(SGLT1)缺失会损害由葡萄糖触发的GLP-1和GIP峰值水平。GLP-1R的生物学特性● GLP-1R的结构特征：属于G蛋白偶联受体(GPCR)，具有典型的七跨膜结构，包含细胞外N端结构域(NTD，负责配体结合)和跨膜结构域(TMD，负责触发受体激活后的信号传导)。● GLP-1R的组织分布：广泛表达于胰腺α、β、δ细胞，以及肠道、胃、心脏、肾脏、中枢神经系统等组织，介导多种生理效应。其中，胰腺β细胞上的GLP-1R是调节胰岛素分泌的关键靶点，而中枢神经系统中的GLP-1R则参与食欲控制和血糖调节。02GLP-1/GLP-1R的功能与信号调控GLP-1/GLP-1R的生理功能●调节血糖：以葡萄糖依赖的方式增强胰岛素分泌、抑制胰高血糖素释放，维持血糖稳定。图1 GLP-1/GLP-1R促进胰岛素分泌、抑制胰高血糖素释放的作用机制●能量代谢：作用于下丘脑神经元，减少食物摄入，并激活棕色脂肪组织产热，促进脂质氧化。●心血管保护：改善血管内皮功能，降低血压和血脂，减少动脉粥样硬化风险。●神经保护：促进神经元存活，抑制炎症和氧化应激，可能改善认知功能。●骨骼与肌肉调节：抑制破骨细胞活性，促进成骨细胞分化，并改善肌肉胰岛素敏感性。●其他作用：可延缓胃排空、抑制食欲，减少食物摄入，从而有助于体重减轻。GLP-1/GLP-1R的作用机制与信号调控●GLP-1/GLP-1R的相关信号通路：通过G蛋白介导cAMP生成，激活PKA、EPAC等下游分子，调控胰岛素分泌、细胞存活和炎症反应；还可通过PI3K/Akt通路促进葡萄糖摄取和β细胞增殖。图2 GLP-1/GLP-1R的相关信号通路●GLP-1/GLP-1R对胰腺细胞的作用①β细胞：GLP-1R激活后通过Gαs蛋白升高细胞内cAMP，激活PKA，促进胰岛素基因表达及分泌；同时通过PI3K/Akt通路促进β细胞增殖、抑制凋亡，增加β细胞数量。图3 GLP-1/GLP-1R促进β细胞增殖、抑制凋亡的作用机制②α细胞：GLP-1R直接作用于α细胞，通过PKA抑制P/Q型Ca²⁺通道，减少胰高血糖素分泌；此外，β细胞分泌的胰岛素和δ细胞分泌的生长抑素(通过旁分泌)也可间接抑制α细胞功能。③δ细胞：GLP-1R激活促进生长抑素分泌，通过抑制α细胞和β细胞的激素释放，形成多层抑制机制。图4 GLP-1/GLP-1R在α细胞、β细胞和δ细胞上降低血糖的作用机制●GLP-1/GLP-1R的信号调控：microRNA(miRNA)通过结合GLP-1R的3'UTR区域，调控其表达及下游信号通路。表2 miRNA在调节GLP-1/GLP-1R信号传导中的作用03GLP-1RAs的分类与作用机制GLP-1RAs的优势GLP-1受体激动剂(GLP-1RAs)的结构与天然GLP-1存在差异，不易被二肽基肽酶-4(DPP-4)降解，作用时间延长，是一类新型降糖药物。相比其他非胰岛素降糖药，能有效降低血糖和糖化血红蛋白(HbA1c)，还能保护心血管、神经系统和肾功能，且不引起低血糖和体重增加。表3 非胰岛素降糖药的作用特点GLP-1RAs的分类●短效激动剂：如贝那鲁肽(Beinaglutide)、艾塞那肽(Exenatide)等。需每日注射2-3次，主要通过显著减慢胃排空，减少葡萄糖吸收，从而降低餐后血糖。●长效激动剂：能持续增强胰岛素分泌、降低胰高血糖素水平，降低空腹血糖并显著减重。①每日一次：利拉鲁肽(Liraglutide)、利西拉来(Lixisenatide)，半衰期13-24小时。②每周一次：司美格鲁肽(Semaglutide)、度拉糖肽(Dulaglutide)，半衰期长达100小时以上。●新型多靶点激动剂：替尔泊肽(Tirzepatide，GLP-1R/GIPR双靶点)、瑞他鲁肽(Retatrutide，GLP-1R/GIPR/GCGR三靶点)，在降糖和减重上效果更优。表4 GLP-1RAs在临床试验中的疗效和安全性概述GLP-1RAs的作用机制● 依赖GLP-1受体途径：与GLP-1受体结合形成复合物，激活G蛋白，进而激活腺苷酸环化酶，催化生成环磷酸腺苷(cAMP)，激活蛋白激酶A等一系列蛋白，影响离子通道、催化下游蛋白磷酸化，发挥多种生物学效应。①cAMP/PKA通路：激活CREB，促进胰岛素基因表达和分泌。②ERK1/2通路：调控细胞增殖与存活，改善β细胞功能。③AMPK通路：促进葡萄糖摄取和脂肪酸氧化，增强胰岛素敏感性。图5 GLP-1RAs的作用机制● 非依赖GLP-1受体途径：①与其他同源受体结合：可能与胰高血糖素受体超家族、胰岛素受体、GIP(葡萄糖依赖性促胰岛素多肽)受体等结构相似的受体结合发挥作用。②与代谢产物的作用：GLP-1的代谢产物如GLP-1(9-36)、GLP-1(28-37)等，可独立于GLP-1受体发挥生物学功能，如在心肾保护中起作用。③与感觉神经元相互作用：作用于表达GLP-1受体的感觉神经元，通过神经传导对其他器官产生生物学效应。表5 不同类型的GLP-1RAs的比较GLP-1RAs对免疫细胞的影响●巨噬细胞①促进M2型极化：GLP-1RAs可促进巨噬细胞向抗炎性M2表型极化，抑制STAT1并激活STAT3，减少促炎因子(如IL-12、TNF-α)分泌，削弱抗肿瘤免疫及疫苗反应。②影响迁移与功能：GLP-1RAs通过cAMP-PKA-STAT3通路增强M2巨噬细胞迁移至炎症部位，可能干扰抗原呈递细胞向淋巴结的迁移。③肝脏巨噬细胞调控：在非酒精性脂肪肝模型中，GLP-1RA可通过极化肝巨噬细胞(库普弗细胞)减轻炎症，但可能抑制局部免疫响应。● T淋巴细胞与NK细胞①Tregs细胞诱导与功能增强：GLP-1RAs可促进Tregs细胞增殖，抑制Th17细胞分化，通过PD-1/PD-L1通路增强免疫抑制，可能降低疫苗诱导的效应T细胞反应。②T细胞无能与耗竭：GLP-1RAs可激活GLP-1R诱导T细胞耗竭标志物表达，抑制TCR激活后的增殖和细胞因子分泌。③iNKT细胞抑制：在银屑病患者中，GLP-1RAs可减少皮肤中不变自然杀伤T(iNKT)细胞数量及细胞因子(IFN-γ、IL-4)分泌，可能影响病毒疫苗的糖脂抗原应答。④肠道T细胞调控：GLP-1RAs可抑制肠道上皮内淋巴细胞(IELs)的细胞因子表达，减轻全身及肠道炎症，但可能削弱口服疫苗依赖的局部T细胞反应。● 其他免疫细胞①中性粒细胞与嗜酸性粒细胞：正常情况下GLP-1R表达量低，但GLP-1RAs可抑制其活化，减少CD11b表达及IL-4、IL-13释放，可能影响局部炎症微环境。②树突状细胞(DC)：GLP-1RAs可能通过抑制TLR介导的细胞因子释放(如TLR1-5、7-9)，削弱DC的抗原呈递能力。GLP-1RAs对其他系统的影响GLP-1RAs通过调节自主神经系统、脂肪、肌肉及肝脏等的代谢信号，形成跨系统的免疫调节网络。● 自主神经系统调控：GLP-1RAs通过中枢神经系统(如后脑、下丘脑)调节自主神经对淋巴结的支配，影响神经递质(如去甲肾上腺素)释放，进而调控免疫细胞活化与迁移。● 脂肪组织：GLP-1RAs促进脂肪细胞棕色化、增加UCP1表达，减轻内质网应激与炎症，同时降低瘦素水平。● 肌肉：GLP-1RAs导致的肌肉萎缩可能影响抗原储存和局部免疫细胞募集。● 肝脏：GLP-1RAs可通过AMPK通路抑制肝脏脂质合成，可能间接影响免疫细胞代谢。● 凝血功能：GLP-1RAs激活血小板GLP-1R可抑制血栓形成，降低疫苗相关凝血不良反应风险。● 延缓胃排空：GLP-1RAs可降低胃窦和十二指肠收缩力、增加幽门张力，抑制迷走神经胆碱能功能，通过回肠制动机制延缓胃排空，延长食物在胃和小肠的停留时间，降低餐后血糖水平。● 调节食欲和饱腹感：GLP-1RAs作用于下丘脑弓状核表达POMC/CART的神经元，直接刺激这些神经元并间接抑制NPY和AgRP神经传递，增加饱腹感、减少饥饿感，从而降低能量摄入，促进体重减轻。图6 GLP-1RAs的生物学效应04GLP-1RAs在多领域的临床应用改善代谢相关疾病● 2型糖尿病(T2D)①作用机制：可显著降低糖化血红蛋白(HbA1c)水平，改善β细胞功能，以葡萄糖依赖的方式促进胰岛素分泌、抑制胰高血糖素释放，还能延缓胃排空、抑制食欲，从而降低血糖。②临床效果：度拉糖肽治疗52周后，患者HbA1c可降低1.5%左右；司美格鲁肽能使HbA1c降低1.8%-2.4%，且降糖效果优于部分传统降糖药物。● 肥胖①作用机制：作用于中枢神经系统，抑制食欲，同时延缓胃排空，增加饱腹感，减少热量摄入，能有效减轻体重。②临床效果：利拉鲁肽3.0mg剂量可使体重下降8%-10%；司美格鲁肽在临床试验中，患者体重可降低15%以上，且减重效果在不同人群中均有体现。● 非酒精性脂肪性肝病(NAFLD)①作用机制：通过改善胰岛素抵抗、调节脂质代谢、减轻肝脏炎症和氧化应激，减少肝脏脂肪堆积，改善肝功能。②临床效果：在动物模型和临床研究中，均显示出对NAFLD的有益作用。例如，替尔泊肽可使肝脂肪含量降低20%-30%；利拉鲁肽能改善肝功能指标，如丙氨酸氨基转移酶(ALT)和天冬氨酸氨基转移酶(AST)水平。● 多囊卵巢综合征(PCOS)：能减轻体重和肥胖，改善胰岛素抵抗和高雄激素血症，恢复发情周期和卵巢形态，提高妊娠率，减轻肝脏和心血管异常。图7 GLP-1RAs对PCOS的有益影响癌症(存在争议)● 作用机制①直接作用：部分肿瘤细胞(如子宫内膜癌、口腔鳞癌细胞)表达GLP-1R，GLP-1RAs可直接抑制其增殖或诱导凋亡。②间接作用：通过调节宿主代谢微环境，如降低胰岛素和胰岛素样生长因子-1(IGF-1)水平，减少促肿瘤信号；或通过抗炎、抗氧化应激作用，抑制肿瘤进展。图8 GLP-1RAs(Liraglutide和Exendin-4)在癌症中的作用机制表6 GLP-1RAs在不同类型癌症中的作用● 动物模型中的抗肿瘤效应①子宫内膜癌：替尔泊肽在肥胖诱导的子宫内膜癌小鼠模型中，显著降低肿瘤重量，且无论小鼠是否喂食高脂饮食，效果均成立。②乳腺癌：司美格鲁肽在乳腺癌原位移植模型中，减少肿瘤体积及肝转移，并通过增强抗肿瘤免疫反应(如促进T细胞浸润)发挥作用。③胰腺癌与三阴性乳腺癌：瑞他鲁肽在胰腺癌模型中降低肿瘤体积，且与吉西他滨联合使用时效果更显著；在肥胖型三阴性乳腺癌模型中，通过抑制YAP蛋白的糖基化与泛素化交互作用，克服治疗耐药性。④口腔鳞癌：司美格鲁肽可剂量依赖性抑制口腔鳞癌细胞的增殖、迁移和存活，机制与P38/MAPK信号通路抑制相关。⑤前列腺癌：多项种研究表明，与磺酰脲类、DPP-4抑制剂、SGLT-2抑制剂及胰岛素相比，GLP-1RAs显著降低前列腺癌的发生率。表7 GLP-1RAs在体外研究中对癌症的影响表8 GLP-1RAs在体内研究中对癌症的影响● 潜在风险：动物实验提示可能增加甲状腺髓样癌和甲状腺癌的风险，但临床证据尚不明确，需进一步研究。免疫介导炎症性疾病(IMIDs)● 炎症性肠病(IBD)：GLP-1RAs可通过抑制NF-κB、PI3K/AKT等促炎通路，促进IL-22分泌，调节肠道菌群(如增加乳酸杆菌)及增强肠屏障功能(上调紧密连接蛋白)来改善肠道炎症。● 银屑病(PsO)：GLP-1RAs通过增加iNKT细胞比例、抑制γδT细胞浸润，下调皮损处IL-17、IL-23等促炎因子发挥作用。临床研究表明，利拉鲁肽、司美格鲁肽等可显著降低PASI评分，改善皮损，且减重与抗炎效应可能协同起效。● 类风湿关节炎(RA)：体外研究发现，GLP-1RAs能抑制RA患者成纤维样滑膜细胞的p38/MAPK、NF-κB通路，减少ROS及MMPs生成，缓解细胞氧化应激与炎症损伤，但目前缺乏临床研究验证其疗效。表9 GLP-1RAs对IMIDs影响的人体体外研究表10 GLP-1RAs对IMIDs影响的人体体内研究神经退行性疾病● 阿尔茨海默病(AD)①作用机制：减少APP/PS1小鼠模型中的β-淀粉样斑块和神经原纤维缠结，改善记忆障碍，降低AD相关炎症蛋白水平，可能通过调节神经炎症和促进神经元存活发挥作用。②临床效果：动物实验显示，利拉鲁肽可减少APP/PS1小鼠模型中的β-淀粉样蛋白沉积，改善认知功能；lixisenatide在部分临床研究中对AD患者的认知功能有改善趋势，但临床证据尚需进一步积累。● 帕金森病(PD)①作用机制：能减少MPTP诱导的小鼠多巴胺能神经元退化，抑制α-突触核蛋白聚集，改善运动功能，可能与抗氧化、抗炎和促进神经元保护信号有关。②临床效果：利拉鲁肽在早期PD患者的临床试验中，对运动功能有一定改善作用；利司那肽也显示出延缓PD进展的潜力，但大规模、长期的临床研究仍需开展。● 亨廷顿病(HD)：GLP-1RAs可减轻3-硝基丙酸诱导的大鼠HD模型的神经行为异常和组织病理改变，延长小鼠生存时间。图9 GLP-1RAs对神经系统的影响心血管疾病● 动脉粥样硬化①作用机制：可减轻血管壁炎症，抑制巨噬细胞泡沫细胞形成，减少动脉粥样硬化斑块破裂，改善脂蛋白和脂质异常，降低心血管疾病风险。②临床效果：多项研究表明，GLP-1RAs可降低低密度脂蛋白胆固醇(LDL-C)10%-15%，减少甘油三酯水平。如利拉鲁肽可使主要不良心血管事件(MACE)风险降低13%；司美格鲁肽在心血管结局试验中，显著降低了心血管死亡、非致死性心肌梗死或非致死性卒中的复合终点风险。图10 GLP-1RAs对颈动脉体活化的影响● 心力衰竭①作用机制：减轻心肌纤维化和肥厚，减少心外膜脂肪沉积，降低炎症介质释放，改善心肌能量代谢。②临床效果：司美格鲁肽在射血分数保留的心力衰竭(HFpEF)患者中，可改善症状和运动功能，提高生活质量评分；利拉鲁肽也被发现对心力衰竭患者的心脏功能有一定保护作用。图11 GLP-1RA、双重或三重激动剂的心血管益处表11 GLP-1RAs对CVD结局影响的临床试验肌肉骨骼系统疾病● 骨质疏松①作用机制：抑制破骨细胞生成，促进成骨细胞增殖和分化，增加骨形成，减少骨吸收，降低骨折风险。②临床效果：艾塞那肽可提高去卵巢大鼠的骨密度，增加骨小梁数量和厚度；利拉鲁肽在部分研究中显示出对骨代谢的有益影响，降低骨折风险。图12 GLP-1RAs对破骨细胞和成骨细胞的影响● 骨关节炎(OA)①作用机制：抑制软骨细胞凋亡，减轻炎症反应，减少关节软骨降解酶的表达，如基质金属蛋白酶(MMPs)和ADAMTS5，从而保护关节软骨。②临床效果：动物实验表明，利拉鲁肽可减轻大鼠OA模型的关节炎症和软骨损伤，降低OARSI评分；在人类研究中，GLP-1RAs对OA患者的疼痛和关节功能有改善作用。图13 GLP-1RAs对肌肉骨骼系统的影响缺血再灌注损伤(IRI)● 心肌缺血再灌注损伤(MIRI)：GLP-1RAs可改善心肌梗死后小鼠的生存状况，减少梗死面积和心脏破裂，减轻离体心脏的IRI，促进梗死心肌血管生成，改善心脏功能。● 脑缺血再灌注损伤(CIRI)：GLP-1RAs能减少大鼠全脑缺血再灌注模型的梗死面积，改善神经行为功能，降低氧化应激、凋亡标志物和炎症因子水平。● 肝缺血再灌注损伤(HIRI)：GLP-1RAs可降低小鼠血清丙氨酸氨基转移酶和天冬氨酸氨基转移酶水平，减少炎症细胞因子，抑制巨噬细胞向促炎表型极化。● 其他器官IRI：GLP-1RAs对肾脏、肠道、胃等器官的IRI也有保护作用，可改善肾功能，减轻组织损伤和细胞凋亡。物质使用障碍● 酒精使用障碍(AUD)：GLP-1RAs可显著减少大鼠的酒精消耗量，抑制小鼠寻求酒精的动机，改善AUD患者症状。● 尼古丁使用障碍：GLP-1RAs可降低小鼠尼古丁消耗量，减少大鼠尼古丁自我给药和寻求动机，改善戒断症状。● 阿片类药物使用障碍：GLP-1RAs可减少大鼠芬太尼、海洛因自我给药和寻求动机，抑制羟考酮自我给药行为。其他疾病● 肾脏疾病①作用机制：减轻缺血和肾毒性物质诱导的急性肾损伤，延缓慢性肾病进展，改善肾功能，减少蛋白尿。②临床效果：在动物实验中，GLP-1RAs可降低血清肌酐和尿素氮水平，减轻肾脏组织损伤(如肾小球硬化和肾小管纤维化)；部分临床研究显示，利拉鲁肽和司美格鲁肽对糖尿病肾病患者的肾功能有保护作用，减少蛋白尿排泄。图14 GLP-1RAs的肾脏保护机制表12 GLP-1RAs和肾脏炎症的临床前研究● 肠道微生物群①作用机制：改变肠道微生物群组成，改善微生物群失调，可能通过调节肠道菌群发挥对代谢和其他疾病的有益作用。②临床意义：肠道微生物群的改善可能与GLP-1RAs的降糖、减重效果及对其他疾病的治疗作用相关，但具体机制仍需深入研究。● 器官移植①作用机制：延长移植物存活时间，减轻心脏移植血管病变和纤维化，可能通过调节T细胞功能抑制排斥反应。②临床前景：动物实验显示，GLP-1RAs可延长心脏移植物的存活时间，但目前相关研究较少，缺乏足够临床证据。抗体发现服务 & 产品01羊驼免疫&骆驼免疫—自建现代化养殖农场02万亿级天然抗体库产品—轻松DIY科研抗体03配套产品—助您轻松搭建基因工程抗体平台关于仁域生物成都仁域生物成立于2019年1月，是一家专注基因工程抗体技术和天然抗体库开发的公司，拥有优化的噬菌体展示抗体库技术和现代化的骆驼/羊驼养殖免疫基地。可为客户提供14天、100%成功率的先导抗体分子发现服务，彻底解决传统抗体定制的周期长、失败率高、成本高三大难题。目前已经成功完成300+靶点抗体筛选项目！protocol 获取 / 产品咨询邮箱｜find@renyubio.com电话｜19136178673地址｜成都市经开区科技产业孵化园关注我们，小编将持续更新相关内容～参考文献Miousse IR. GLP-1 receptor agonists in the context of cancer: the road ahead. Am J Physiol Cell Physiol. 2025 Jun 1;328(6):C1822-C1828. Li S, Huang N, Wang M, Huang W, Luo Y, Huang J. GLP-1R in diabetes mellitus: from basic discovery to therapeutics development. Front Pharmacol. 2025 May 30;16:1610512.J C, Me C, Mt C. Renoprotective mechanisms of glucagon-like peptide-1 receptor agonists. Diabetes Metab. 2025 May;51(3):101641. Thin L, Teh WL. GLP-1R Agonists and Their Therapeutic Potential in Inflammatory Bowel Disease and Other Immune-Mediated Inflammatory Diseases, a Systematic Review of the Literature. Biomedicines. 2025 May 6;13(5):1128. Si J, Yu K, Hao J, Wang J, Zhang L. The therapeutic effects and mechanisms of glucagon-like peptide-1 receptor agonists in neurocognitive disorders. Ther Adv Neurol Disord. 2025 Apr 17;18:17562864251332035.Urkon M, Ferencz E, Szász JA, Szabo MIM, Orbán-Kis K, Szatmári S, Nagy EE. Antidiabetic GLP-1 Receptor Agonists Have Neuroprotective Properties in Experimental Animal Models of Alzheimer's Disease. Pharmaceuticals (Basel). 2025 Apr 23;18(5):614. Al-Noshokaty TM, Abdelhamid R, Abdelmaksoud NM, Khaled A, Hossam M, Ahmed R, Saber T, Khaled S, Elshaer SS, Abulsoud AI. Unlocking the multifaceted roles of GLP-1: Physiological functions and therapeutic potential. Toxicol Rep. 2025 Jan 16;14:101895. He X, Zhao W, Li P, Zhang Y, Li G, Su H, Lu B, Pang Z. Research progress of GLP-1RAs in the treatment of type 2 diabetes mellitus. Front Pharmacol. 2025 Jan 20;15:1483792.Lu C, Xu C, Yang J. The Beneficial Effects of GLP-1 Receptor Agonists Other than Their Anti-Diabetic and Anti-Obesity Properties. Medicina (Kaunas). 2024 Dec 26;61(1):17. Ibrahim SS, Ibrahim RS, Arabi B, Brockmueller A, Shakibaei M, Büsselberg D. The effect of GLP-1R agonists on the medical triad of obesity, diabetes, and cancer. Cancer Metastasis Rev. 2024 Dec;43(4):1297-1314.Yu X, Liu J. Effect of glucagon-like peptide-1 receptor agonists on prostate cancer: A review. Medicine (Baltimore). 2024 Oct 11;103(41):e39956. Yu X, Liu J. Effect of glucagon-like peptide-1 receptor agonists on prostate cancer: A review. Medicine (Baltimore). 2024 Oct 11;103(41):e39956.Zheng Z, Zong Y, Ma Y, Tian Y, Pang Y, Zhang C, Gao J. Glucagon-like peptide-1 receptor: mechanisms and advances in therapy. Signal Transduct Target Ther. 2024 Sep 18;9(1):234. Mullur N, Morissette A, Morrow NM, Mulvihill EE. GLP-1 receptor agonist-based therapies and cardiovascular risk: a review of mechanisms. J Endocrinol. 2024 Sep 19;263(1):e240046.Trakoonsenathong R, Chiu CF, Saengboonmee C. Glucagon-like peptide 1 receptor agonist: A potential game changer for cholangiocarcinoma. World J Gastroenterol. 2024 Sep 14;30(34):3862-3867. van Niekerk G, Coelmont L, Alpizar YA, Kelchtermans L, Broeckhoven E, Dallmeier K. GLP-1R agonist therapy and vaccine response: Neglected implications. 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临床结果

100 项与羟考酮相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D05312	羟考酮	N02AA05	DB00497

研发状态

批准上市

10 条最早获批的记录,

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适应症	国家/地区	公司	日期
疼痛	中国	Napp Pharmaceutical Holdings Ltd.	2004-01-21

未上市

10 条进展最快的记录,

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适应症	最高研发状态	国家/地区	公司	日期
癌症疼痛	临床3期	-	萌蒂（中国）制药有限公司	2011-01-01
肿瘤	临床3期	-	萌蒂（中国）制药有限公司	2011-01-01
术后疼痛	临床3期	中国	萌蒂（中国）制药有限公司	2010-03-01
骨关节炎	临床3期	比利时	Mundipharma Research GmbH & Co. KG	2009-05-01
骨关节炎	临床3期	捷克	Mundipharma Research GmbH & Co. KG	2009-05-01
骨关节炎	临床3期	芬兰	Mundipharma Research GmbH & Co. KG	2009-05-01
骨关节炎	临床3期	德国	Mundipharma Research GmbH & Co. KG	2009-05-01
骨关节炎	临床3期	匈牙利	Mundipharma Research GmbH & Co. KG	2009-05-01
骨关节炎	临床3期	西班牙	Mundipharma Research GmbH & Co. KG	2009-05-01
急性疼痛	临床2期	美国	Ensysce Biosciences, Inc.	2023-10-05

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临床结果

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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


NCT05470465 (CTgov)	临床1期	高碳酸血症	27	Placebo+Oxycodone (Treatment A: Placebo)	壓齋餘遞齋鑰醖糧獵獵(遞網鏇顧艱鏇簾衊簾鹹) = 鹹糧觸選夢選獵憲簾遞獵膚襯夢壓鹹顧襯範築 (淵壓網選築糧憲積觸遞, 齋襯衊淵鏇餘廠網製鑰 ~ 製顧餘繭鹹衊選遞遞窪) 更多	-	2025-05-22
				Paroxetine+Oxycodone (Treatment B: Paroxetine)	壓齋餘遞齋鑰醖糧獵獵(遞網鏇顧艱鏇簾衊簾鹹) = 糧鹽構製艱鹽製憲鬱顧獵膚襯夢壓鹹顧襯範築 (淵壓網選築糧憲積觸遞, 襯憲蓋膚壓壓遞觸襯選 ~ 繭廠鏇醖窪願齋觸鬱獵) 更多
NCT05924165 (CTgov)	临床4期	肾石病	90	5mg Oxycodone, Q6 PRN (Opioid Group)	窪網範鹹選蓋繭膚夢選(醖餘襯繭齋夢夢願夢簾) = 鏇鏇齋繭醖艱鏇鹹獵膚願網齋鑰積築膚獵艱齋 (遞鏇窪夢構鹽繭壓艱廠, 憲憲窪範積鏇壓構繭糧 ~ 淵顧觸鑰廠鏇範構齋衊) 更多	-	2025-03-26
				10mg Ketorolac, Q6 PRN (NSAID)	窪網範鹹選蓋繭膚夢選(醖餘襯繭齋夢夢願夢簾) = 範廠鏇淵窪鏇襯窪觸鹹願網齋鑰積築膚獵艱齋 (遞鏇窪夢構鹽繭壓艱廠, 獵窪築選艱醖衊選窪顧 ~ 積膚糧襯範網獵廠繭觸) 更多
PF614-MPAR-102 (Company_Website) 人工标引	临床1期	重度疼痛	-	PF614-MPAR	夢觸鑰顧積鏇簾鑰憲淵(觸繭選夢構觸壓餘鏇膚) = MPAR product had a significantly lower (p=0.0019) total maximum blood concentration of oxycodone (Cmax) compared to PF614 alone, an indication of overdose protection. 鏇蓋鬱鹹壓構繭壓鏇齋 (觸醖積鹹襯夢鬱鏇齋膚 ) 更多	积极	2025-01-22
NCT04296396 (Eunice Kennedy Shriver National Institute of Child Health and Human Development Maternal-Fetal Medicine Units Network, Pubmed \| Obstet Gynecol)	临床3期	-	-	Opioid (IOPP with shared decision making)	簾積夢廠衊廠襯鏇壓齋(鏇範願製鏇憲觸觸夢遞) = 簾鹹夢遞顧蓋壓鬱醖糧淵衊築齋鬱窪簾襯觸繭 (鑰餘願淵構繭鹽糧憲鹽 ) 更多	积极	2024-08-01
				Fixed quantity (20 tablets of 5 mg oxycodone)	簾積夢廠衊廠襯鏇壓齋(鏇範願製鏇憲觸觸夢遞) = 艱鹽選觸鏇鑰齋願衊範淵衊築齋鬱窪簾襯觸繭 (鑰餘願淵構繭鹽糧憲鹽 ) 更多
PF614-201 (Biospace) 人工标引	临床2期	-	-	PF614	襯衊鏇淵憲網艱壓鏇範(醖網顧鑰構襯齋糧構鏇) = demonstrated time-to-efficacy onset for the analgesia effect and significant decrease of pain intensity versus placebo of PF614 at two different dose levels 鬱鹽衊壓築顧範餘憲窪 (鬱選構艱鑰壓顧鏇壓壓 )	积极	2023-12-14
				placebo
WSC2023	N/A	-	-	Opioid medications	願餘簾襯積蓋齋餘鬱願(鏇夢艱窪顧膚鏇蓋積構) = 憲壓憲壓構鏇廠淵醖鹽醖夢餘範繭網選選夢顧 (願構夢遞簾製鏇醖廠鑰 )	-	2023-10-23
EHA2023	N/A	肿瘤	-	Oxycodone	願壓鏇憲夢襯鹽鹹願選(網糧衊獵製鑰選艱顧築) = 簾廠願憲觸夢窪壓鹹構襯夢選膚顧範顧艱夢積 (鹽膚膚鹽憲蓋範鬱壓廠 )	-	2023-06-08
				Morphine	願壓鏇憲夢襯鹽鹹願選(網糧衊獵製鑰選艱顧築) = 餘簾壓顧膚膚鹽簾製蓋襯夢選膚顧範顧艱夢積 (鹽膚膚鹽憲蓋範鬱壓廠 )
NCT05567354 (HAP, Corporate Publications) 人工标引	临床1期	慢性疼痛	26	PF614	製蓋艱簾衊鹹窪艱襯膚(顧廠衊艱糧壓蓋齋艱範): P-Value = 0.0133 更多	积极	2022-10-31
				crushed oxycodone
UEGW2022	N/A	-	-	opioid analgesia (Anterograde DAE)	網構憲蓋衊鹹糧廠艱鹽(窪蓋網衊壓遞繭艱繭鏇) = 範觸夢繭壓願製鑰顧廠製壓鏇遞築鹽淵餘壓網 (襯願蓋網獵襯壓鬱鏇顧 ) 更多	-	2022-10-09
				opioid analgesia (Retrograde DAE)	網構憲蓋衊鹹糧廠艱鹽(窪蓋網衊壓遞繭艱繭鏇) = 衊醖築衊鬱繭範顧簾壓製壓鏇遞築鹽淵餘壓網 (襯願蓋網獵襯壓鬱鏇顧 ) 更多
SGO2022	N/A	-	-	opioid (Open Surgery)	選範鏇繭鬱顧構齋繭製(壓夢網膚鹽選獵製憲選) = 構窪網夢範觸構網選簾鑰憲艱顧齋網糧簾顧構 (夢餘壓範築繭窪鹹憲範, 1 ~ 19)	-	2022-08-01