Probenecid

- Late-Breaking Phase 3 Data from the IDEAL Study Highlight the Impact of Livdelzi ® on Composite Alkaline Phosphatase (ALP) Normalization and Other Markers of Disease Progression in Primary Biliary Cholangitis (PBC) - - New Long-Term and Real-World Evidence in Hepatitis Delta Virus (HDV) Examine Combined Virologic and Biochemical Response with Hepcludex ® - FOSTER CITY, Calif.--(BUSINESS WIRE)--Gilead Sciences, Inc. (Nasdaq: GILD) will present new clinical and real-world evidence across primary biliary cholangitis (PBC) and chronic hepatitis delta virus (HDV) infection at The Liver Meeting ® 2026, hosted by the American Association for the Study of Liver Diseases (AASLD), November 5-9 in Denver, Colorado. The data will examine durability of response, patient-relevant symptoms, and opportunities to better understand long-term disease management across these two rare and serious liver diseases. Key Highlights Gilead’s scientific program includes 21 accepted abstracts, including late-breaking Phase 3 research from the Livdelzi ® (seladelpar) 10 mg development program and new long-term and real-world evidence for Hepcludex ® (bulevirtide-gmod) 2 mg and 8.5 mg in chronic HDV. The portfolio of research reflects Gilead's continued focus on generating evidence that helps broaden understanding of treatment response, patient experience, and long-term management considerations. By combining long-term clinical data, real-world insights, and research in patient-centred outcomes, Gilead continues to drive innovation and progress scientific advancements to inform treatment decisions and enhance understanding of rare liver diseases. Improving Care Across the PBC Journey Gilead will present analyses from the Livdelzi clinical development program and real-world studies, including late-breaking Phase 3 presentation of the IDEAL study results which evaluate the impact of seladelpar on composite alkaline phosphatase (ALP) normalization in a historically understudied population of adults living with PBC with lower levels of ALP elevation (1-1.67x ULN) who were on or intolerant to ursodeoxycholic acid (UCDA). (LB#5007). ALP normalization is an increasingly recognized treatment goal that continues to be studied in relation to long-term outcomes in PBC. Additional data on safety and efficacy of seladelpar up to five years (#1170) and late-breaking data on fatigue (LB#5040) will also be presented. Additional real-world studies will examine persistent gaps in care, including factors affecting eligibility for, and escalation to, second-line treatment (#1170 and #1221). Together, the analyses provide a broader understanding of the diverse experiences, unmet needs and challenges faced by people living with PBC, including those at high risk of disease progression. “As treatment options evolve, our ambitions for people living with rare liver diseases should evolve as well,” said Swati Tole, Senior Vice President, Clinical Development, Inflammation at Gilead. “At The Liver Meeting, we will present late-breaking results from the Phase 3 IDEAL study highlighting composite alkaline phosphatase (ALP) normalization, an important marker of disease activity in people with PBC. We will also share data that look beyond biochemical measures of disease activity to explore durability of response, symptoms and the realities of long-term disease management. Together, these insights can help broaden our understanding of important aspects of care for people living with PBC.” Advancing Long-Term Disease Outcomes in Chronic HDV Gilead will also present new long-term and real-world data that deepens the understanding of Hepcludex for the treatment of chronic HDV. Highlights include 96-week efficacy findings on the combined virologic and biochemical response (#3203) and a 48-week analysis of clinically significant portal hypertension prevalence and impact of Hepcludex in people living with chronic HDV (#3243). U.S. real-world studies will also spotlight low testing rates (#4080) and the burden of advanced liver disease (#3216), underscoring the need for earlier detection and stronger long-term management for people living with HDV. Gilead’s Commitment to Improving Outcomes for People with Liver Diseases For people living with PBC and HDV, delayed diagnosis and treatment can mean more time living with burdensome symptoms or progressive liver damage. Gilead's new data highlight these persistent gaps and showcase opportunities for earlier diagnosis, timely treatment escalation, more patient-centered research, and a better understanding of long-term disease management. Collectively, the data emphasizes the importance of identifying people at risk of progression, optimizing treatment decisions and advancing understanding of long-term outcomes across PBC and HDV. For more information, including a complete list of abstract titles being presented at the meeting, please visit the AASLD website . Key Abstracts at AASLD 2026: ID Abstract Title PBC Abstract #5007 Oral Presentation November 8, 2026 5:00–5:15 PM Seladelpar for Alkaline Phosphatase Normalization in Primary Biliary Cholangitis: Results from the IDEAL Phase III Randomized-Controlled Trial Abstract #5040 Poster Presentation November 8, 2026 1:00–2:00 PM Clinically Meaningful Fatigue Improvement with Seladelpar in Patients with Primary Biliary Cholangitis: Data from the Open-label ASSURE Study Abstract #1170 Poster Session November 5, 2026 12:00-1:00 PM Sustained Biochemical Efficacy and Safety of Seladelpar in Patients with Primary Biliary Cholangitis, Including Those at High Risk for Progression, up to 5 years of Treatment from ASSURE Abstract #1137 Poster Session November 5, 2026 12:00-1:00 PM Seladelpar is Associated with Stable Renal Function Over 5 Years of Treatment: Interim Results from the ASSURE Study Abstract #1164 Poster Session November 5, 2026 12:00-1:00 PM Seladelpar Downregulates Inflammatory and Fibrotic Pathways: Insights from Serum Proteomic Analysis Abstract #1157 Poster Session November 5, 2026 12:00-1:00 PM Seladelpar Leads to Rapid and Sustained Alkaline Phosphatase Reduction, Regardless of Baseline Levels, Over 5 Years of Treatment in Patients with Primary Biliary Cholangitis Abstract #1160 Poster Session November 5, 2026 12:00-1:00 PM Seladelpar Leads to Long-Term Efficacy and Safety in Patients with Prior OCA and/or Fibrate Exposure Abstract #1233 Poster Session November 5, 2026 12:00-1:00 PM Seladelpar Leads to Durable and Significant Decrease in the Pruritogenic Cytokine IL-31, Associated with Pruritus Improvement: Long-Term Data from the ASSURE Study Abstract #1221 Poster Session November 5, 2026 12:00-1:00 PM Risk Factors for Progression in Patients with Primary Biliary Cholangitis who are Eligible for Second-line Treatment: Evidence from a Real-world Study Abstract #1171 Poster Session November 5, 2026 12:00-1:00 PM Health-related Quality of Life Among Patients with PBC by Response Status: Analysis of a Real-world Dataset Abstract #1182 Poster Session November 5, 2026 12:00-1:00 PM Healthcare Resource Utilization and Costs in Patients with Primary Biliary Cholangitis in the United States Abstract #1313 Poster Session November 5, 2026 12:00-1:00 PM Association Between Treatment Adherence and Healthcare Utilization Among Individuals with Primary Biliary Cholangitis in the United States Hepatitis Delta Abstract #3200 Poster Session November 7, 2026 1:00–2:00 PM Characteristics and Outcomes of On-Treatment ALT Flares in Patients with Hepatitis Delta Virus Receiving Bulevirtide and Pegylated Interferon Abstract #3203 Poster Session November 7, 2026 1:00–2:00 PM Integrated Efficacy Analysis of Bulevirtide 10 mg Monotherapy in Patients with Chronic Hepatitis Delta Abstract #3243 Poster Session November 7, 2026 1:00–2:00 PM Clinically Significant Portal Hypertension may Improve in Some Patients with Chronic Hepatitis Delta After 48 Weeks of Bulevirtide Treatment - a Pooled Analysis of Phase II/III Clinical Trials Abstract #4080 Poster Session November 8, 2026 1:00–2:00 PM Hepatitis Delta Testing Rates Remain Low Among Individuals with Chronic Hepatitis B: a US Administrative Claims Analysis Abstract #3216 Poster Session November 7, 2026 1:00–2:00 PM Disease Progression Among a Nationally Representative Cohort of Commercially Insured Patients with Hepatitis Delta Virus in the United States Abstract #3215 Poster Session November 7, 2026 1:00–2:00 PM On-Treatment and Posttreatment Patterns of Non-Invasive Tests of Fibrosis with Long-Term Bulevirtide Treatment for Chronic Hepatitis Delta: An Integrated Analysis Abstract #3236 Poster Session November 7, 2026 1:00–2:00 PM Diagnostic Performance of Noninvasive Tests for Hepatic Fibrosis in Patients with Chronic Hepatitis Delta Receiving Bulevirtide Abstract #3202 Poster Session November 7, 2026 1:00–2:00 PM A Systematic Literature Review and Meta-Analysis Evaluating Post-Treatment HDV RNA-Based Surrogate Endpoints for Predicting Long-Term Clinical Outcomes in Hepatitis Delta Virus Infection Hepatitis B Abstract #4089 Poster Session November 8, 2026 1:00–2:00 PM Combining PAGE-B Score with Fibrotest Improves HCC Risk Stratification in Patients Treated with Tenofovir-based Treatment About Livdelzi Livdelzi (seladelpar) is an oral PPAR‑delta agonist, or delpar, for the treatment of primary biliary cholangitis (PBC). PPAR‑delta is known to regulate key metabolic and liver disease pathways. Preclinical and clinical data indicate that Livdelzi has anticholestatic, anti‑inflammatory, antipruritic, and antifibrotic effects. Clinical trial data demonstrate that Livdelzi supports meaningful improvements in key markers of disease activity, including biochemical response and alkaline phosphatase (ALP) normalization, with sustained effects observed over long‑term follow‑up in multiple studies. These findings are supported by clinical studies evaluating Livdelzi in participants treated for up to 5 years. Livdelzi has the potential to help address ongoing unmet needs for people living with PBC, including those who remain inadequately controlled on existing therapies. Pruritus is one of the most common and debilitating symptoms of PBC that can significantly impair quality of life. Clinical trial data have demonstrated improvements in pruritus with Livdelzi compared with placebo. U.S. Indication for Livdelzi Livdelzi is indicated for the treatment of primary biliary cholangitis (PBC), in combination with ursodeoxycholic acid (UDCA) in adults who have had an inadequate response to UDCA, or as monotherapy in patients unable to tolerate UDCA. This indication is approved under accelerated approval based on a reduction of alkaline phosphatase (ALP). Improvement in survival or prevention of liver decompensation events have not been demonstrated. Continued approval for this indication may be contingent upon verification and description of clinical benefit in confirmatory trial(s). Limitations of Use: Use of Livdelzi is not recommended in patients who have or develop decompensated cirrhosis (e.g., ascites, variceal bleeding, hepatic encephalopathy). U.S. Important Safety Information for LIVDELZI Warnings and Precautions Fractures: Fractures occurred in 4% of LIVDELZI-treated patients compared to no placebo-treated patients. Consider the risk of fracture in the care of patients treated with LIVDELZI and monitor bone health according to current standards of care. Liver Test Abnormalities: LIVDELZI has been associated with dose-related increases in serum transaminase (AST and ALT) levels > 3 x ULN in patients receiving 50 mg and 200 mg once daily (5x and 20x higher than the recommended dosage of 10 mg once daily). Perform baseline clinical and laboratory testing when starting LIVDELZI and monitor thereafter according to routine patient management. Interrupt treatment if the liver tests (ALT, AST, total bilirubin, and/or ALP) worsen, or if the patient develops signs and symptoms of clinical hepatitis (e.g., jaundice, right upper quadrant pain, eosinophilia). Consider permanent discontinuation if liver tests worsen after restarting LIVDELZI. Biliary Obstruction: Avoid use of LIVDELZI in patients with complete biliary obstruction. If biliary obstruction is suspected, interrupt LIVDELZI and treat as clinically indicated. Adverse Reactions The most common adverse reactions (≥5%) with LIVDELZI were headache (8%), abdominal pain (7%), nausea (6%), abdominal distension (6%), and dizziness (5%). Drug Interactions Potential Increased Exposure of LIVDELZI with: Probenecid: Avoid coadministration with LIVDELZI. Strong CYP2C9 Inhibitors: Monitor for adverse effects during concomitant use. Dual Moderate CYP2C9 and Moderate or Strong CYP3A4 Inhibitors (eg, fluconazole): Monitor for adverse effects during concomitant use. CYP2C9 Poor Metabolizers Using Moderate or Strong CYP3A4 Inhibitors: Monitor for adverse effects during concomitant use of a moderate or strong CYP3A4 inhibitor in patients who are CYP2C9 poor metabolizers. Dual or Multiple Clinical Inhibitors of Drug Transporters OATP1B1, OATP1B3, and BCRP (eg, cyclosporine): Monitor for adverse effects during concomitant use. Potential Reduction in LIVDELZI Exposure with: Rifampin: Concomitant use of LIVDELZI with rifampin, an inducer of metabolizing enzymes, may result in delayed or suboptimal LIVDELZI biochemical response. Monitor biochemical response (eg, ALP and bilirubin) when patients initiate rifampin during LIVDELZI treatment. Bile Acid Sequestrants: Administer LIVDELZI at least 4 hours before or 4 hours after taking a bile acid sequestrant, or at as great an interval as possible. Pregnancy and Lactation Pregnancy: There are insufficient data from human pregnancies exposed to LIVDELZI to allow an assessment of a drug-associated risk of major birth defects, miscarriage, or other adverse maternal or fetal outcomes. Report pregnancies to Gilead Sciences, Inc., at 1-800-445-3235. Lactation: There are no data on the presence of LIVDELZI in human milk, the effects on the breastfed infant, or the effects on milk production. The developmental and health benefits of breastfeeding should be considered along with the mother's clinical need for LIVDELZI and any potential adverse effects on the breastfed infant from LIVDELZI. About Hepcludex (bulevirtide-gmod) 8.5 mg in the U.S. Hepcludex (bulevirtide-gmod) is a first-in-class entry inhibitor for the treatment of adults living with chronic hepatitis delta virus (HDV) infection. Chronic HDV infection is a serious liver disease that occurs only as a co-infection in individuals with chronic HBV and is associated with rapid disease progression, liver failure, and increased mortality. Hepcludex is supplied as a vial for once-daily subcutaneous injection. Each vial contains an 8.5 mg dose when prepared according to the Instructions for Use within FDA-approved labeling. Hepcludex works by blocking the entry of both HDV and HBV into liver cells, addressing a key step in the viral lifecycle. The FDA’s accelerated approval of Hepcludex is supported by data from the Phase 3 MYR301 study demonstrating that Hepcludex was an effective and generally well-tolerated treatment option, with efficacy and safety observed at week 48 through long-term treatment of up to 144 weeks. Hepcludex is supplied as a once-daily injectable therapy and represents the first and only treatment option for people living with chronic HDV that received FDA accelerated approval in the United States, addressing a long-standing unmet medical need for this historically underserved patient community. For more information, please visit Hepcludex.com U.S. Access and Hepcludex Approval Across Markets The Gilead Support Path ® Program offers information and resources to help patients diagnosed with chronic HBV, HDV and hepatitis C virus (HCV) and primary biliary cholangitis (PBC), as well as healthcare professionals, understand coverage and financial options for prescribed Gilead treatments. Bulevirtide 2 mg is also approved for use in the European Economic Area (EEA), Canada the United Kingdom and other countries globally to treat people living with chronic HDV. Please see below for U.S. Indication and Important Safety Information for Hepcludex. U.S. Indication for Hepcludex Hepcludex (bulevirtide-gmod) 8.5 mg for injection is indicated for the treatment of chronic hepatitis delta virus infection in adults without cirrhosis or with compensated cirrhosis. This indication is approved under accelerated approval based on a decrease in HDV RNA and alanine aminotransferase (ALT) normalization. An improvement in disease-related clinical outcomes has not been established. Continued approval for this indication may be contingent upon verification and description of clinical benefit in a confirmatory trial(s). U.S. Important Safety Information for HEPCLUDEX IMPORTANT SAFETY INFORMATION BOXED WARNING: POSTTREATMENT SEVERE ACUTE EXACERBATION OF HEPATITIS D and B Severe acute exacerbations of hepatitis D and hepatitis B may occur after HEPCLUDEX is discontinued, especially in patients with cirrhosis, who may be at increased risk of more severe flares or progression to hepatic decompensation. Monitor hepatic function closely with both clinical and laboratory follow-up, including hepatitis B virus (HBV) DNA and hepatitis delta virus (HDV) RNA viral load, for at least six months in patients who discontinue HEPCLUDEX. Resumption of antiviral therapy may be warranted. Warnings and Precautions Hypersensitivity reactions including anaphylaxis: Hypersensitivity reactions, including anaphylaxis, have been reported with HEPCLUDEX. If signs or symptoms of a clinically significant hypersensitivity reaction or anaphylaxis occur, immediately discontinue HEPCLUDEX and initiate appropriate treatment. Adverse Reactions Most common adverse reactions (incidence ≥10%; all grades) in HEPCLUDEX clinical trials were injection site reactions, headache, abdominal pain, fatigue and pruritus. Dosage and Administration Dosage in adults: 8.5 mg once daily administered by subcutaneous injection HEPCLUDEX should be continued as long as it is associated with a response to treatment. The optimal treatment duration is unknown. In all patients, manage the underlying HBV infection as clinically appropriate. Pregnancy and Lactation Pregnancy: There are insufficient data from human pregnancies exposed to HEPCLUDEX to allow an assessment of a drug-associated risk of major birth defects, miscarriage, or other adverse maternal or fetal outcomes. Lactation: There are no data on the presence of HEPCLUDEX in human milk, the effects on the breastfed infant, or the effects on milk production. The developmental and health benefits of breastfeeding should be considered along with the mother's clinical need for HEPCLUDEX and any potential adverse effects on the breastfed child from HEPCLUDEX or from the underlying maternal condition. About Gilead Sciences in Liver Disease For decades, Gilead has pioneered the way forward to improve the lives of people living with liver disease around the world. We have helped to transform hepatitis C from a chronic condition into one that can be cured for millions of people. For individuals living with hepatitis B or D, Gilead's focus on advancing medicines drives hope that today’s research will turn into tomorrow’s cures. Beyond viral hepatitis, Gilead is working to deliver advanced treatments for people living with PBC. But our commitment doesn’t stop there. Through ground-breaking science and collaborative partnerships, we strive to create healthier futures for everyone living with liver disease. Gilead remains committed to a future without liver disease. About Gilead Sciences Gilead Sciences, Inc. is a biopharmaceutical company that has pursued and achieved breakthroughs in medicine for more than three decades, with the goal of creating a healthier world for all people. The company is committed to advancing innovative medicines to prevent and treat life-threatening diseases, including HIV, viral hepatitis, COVID-19, cancer and inflammation. In 2025, Gilead announced a $32 billion investment to further strengthen its U.S. footprint to power the next era of discovery, job creation and public health preparedness – while continuing to invest globally to ensure patients everywhere benefit from its scientific innovation. Gilead operates in more than 35 countries worldwide, with headquarters in Foster City, Calif. Forward-Looking Statements This press release includes forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995 that are subject to risks, uncertainties and other factors, including Gilead’s ability to initiate, progress or complete clinical trials within currently anticipated timelines or at all, and the possibility of unfavorable results from ongoing or additional clinical trials, including those involving Livdelzi/Lyvdelzi (seladelpar) and Hepcludex (bulevirtide) (such as IDEAL); uncertainties relating to regulatory applications and related filing and approval timelines, including additional pending and potential applications for seladelpar and bulevirtide; the risk that any regulatory approvals, if granted, may be subject to significant limitations on use or subject to withdrawal or other adverse actions by the applicable regulatory authority; and any assumptions underlying any of the foregoing. These and other risks, uncertainties and factors are described in detail in Gilead’s Quarterly Report on Form 10-Q for the quarter ended June 30, 2026, as filed with the U.S. Securities and Exchange Commission. These risks, uncertainties and other factors could cause actual results to differ materially from those referred to in the forward-looking statements. All statements other than statements of historical fact are statements that could be deemed forward-looking statements. The reader is cautioned that any such forward-looking statements are not guarantees of future performance and involve risks and uncertainties and is cautioned not to place undue reliance on these forward-looking statements. All forward-looking statements are based on information currently available to Gilead, and Gilead assumes no obligation and disclaims any intent to update any such forward-looking statements. Hepcludex, Livdelzi, Lyvdelzi, Gilead and the Gilead logo are trademarks of Gilead Sciences, Inc., or its related companies. U.S. full Prescribing Information for Livdelzi ® and Hepcludex ® is available at . For more information about Gilead, please visit the company’s website at , follow Gilead on X/Twitter(@Gilead Sciences) and LinkedIn(@Gilead-Sciences) Contacts Priscilla White, Media public_affairs@gilead.com Jacquie Ross, Investors investor_relations@gilead.com

各位备考执业药师的小伙伴，大家好。 《药学专业知识一》是很多考生备考路上的难点，知识点零散、化学结构多、概念易混淆，复习时很难抓住核心。 今天整理了药一300个高频考点精简笔记，把历年考试常考的基础概念、药物结构、代谢特点、药典规定、剂型辅料等内容汇总，剔除冷门偏题，方便大家碎片化复习。✅ 一、药品基础概念考点 药品的通用名也称国际非专利药品名称（INN），也是药典中推荐使用的名称，一个药物只有一个通用名，不受专利和行政保护。 药物的商品名通常针对最终产品，不得冒用顶替。商品名同商标一样可以注册和申请专利保护，只能由该药品的拥有者和制造者使用，不能暗示药物的疗效和用途，应简易顺口。 地西泮为中枢镇静药，结构母核为苯二氮䓬。 阿昔洛韦为抗病毒药，结构母核为鸟嘌呤。 氯丙嗪为抗精神病药，结构母核为吩噻嗪类。 剂型：是适合于疾病的诊断、治疗或预防的需要而制备的不同给药形式。 药物制剂：指将原料药物按照某种剂型制成一定规格并具有一定质量标准的具体品种。💊 给药剂型分类（非胃肠道给药） 注射给药：静脉、肌内、皮下及皮内注射； 皮肤给药：外用溶液剂、洗剂、软膏剂、贴剂、凝胶剂等； 口腔给药：漱口剂、含片、舌下片剂、膜剂； 鼻腔给药：滴鼻剂、喷雾剂、粉雾剂等； 肺部给药：气雾剂、吸入剂、粉雾剂等； 眼部给药：滴眼剂、眼膏剂、眼用凝胶、植入剂等； 直肠、阴道和尿道给药：灌洗剂、栓剂等。 8. 药物剂型的重要性：可改变药物的作用性质、可调节药物的作用速度、可降低（或消除）药物的不良反应、可产生靶向作用、可提高药物的稳定性、可影响疗效。 9. 硫酸镁：口服剂型用作泻下药，但5%注射液静脉滴注，具有镇静、解痉作用。 10. 药用辅料的作用：赋形、使制备过程顺利进行、提高药物稳定性、提高药物疗效、降低药物不良反应、调节药物作用、增加病人用药的顺应性。✅ 二、药物稳定性相关考点⚠️ 易发生水解的药物 酯类：盐酸普鲁卡因、盐酸丁卡因、硫酸阿托品、氢溴酸后马托品、溴丙胺太林、盐酸可卡因； 酰胺（含内酰胺）：对乙酰氨基酚、巴比妥类、利多卡因、青霉素类、头孢菌素类、氯霉素； 其他：阿糖胞苷；维生素B、地西泮、碘苷。⚠️ 易发生氧化的药物 酚类（含酚羟基）：如肾上腺素、左旋多巴、吗啡、水杨酸钠； 烯醇类（烯醇基）：维生素C； 其他类：噻嗪类（盐酸氯丙嗪、盐酸异丙嗪）、芳胺类（磺胺嘧啶钠）、吡唑酮类（氨基比林、安乃近）、维生素A或维生素D等。 14. 药物制剂稳定化方法：控制温度、调节pH、改变溶剂、控制水分及湿度、遮光、驱逐氧气、加入抗氧剂或金属离子络合剂、其他（改进剂型或生产工艺、制成稳定的衍生物、加入干燥剂及改善包装）。 15. 常用的水溶性抗氧剂：①亚硫酸钠、硫代硫酸钠：用于碱性药物溶液；②亚硫酸氢钠、焦亚硫酸钠：用于弱酸性溶液；③硫脲、维生素C、半胱氨酸等。 16. 常用的油溶性抗氧剂：叔丁基对羟基茴香醚（BHA），2，6-二叔丁基对甲酚（BHT）、维生素E。 17. 药品有效期：药物降解10%所需的时间，记作\boldsymbol{t_{0.9}}。公式：\boldsymbol{t_{0.9}=0.1054/k}。✅ 三、《中国药典》相关考点 18. 《中国药典》组成： 一部：药材和饮片、植物油脂和提取物、成方制剂和单味制剂； 二部：化学药品、抗生素和生化药品、放射性药品； 三部：生物制品； 四部：通则和药用辅料。 19. 凡例：是正确使用《中国药典》进行药品质量检定的基本原则，是《中国药典》的重要组成部分，对药典收载的正文与通则的有关规定具有法定的约束力。 20. 紫外-可见分光光度法：吸收波长λ，吸光度A。 21. 红外分光光度法：化合物的红外吸收光谱具有人指纹一样的特征专属性，几乎没有两个化合物具有相同的红外光谱。 22. 色谱鉴别法：用于鉴别的色谱法主要是高效液相色谱法（HPLC），以含量测定项下记录的色谱图中待测成分色谱峰的保留时间（tR）作为鉴别依据。📋 标准物质分类 23. 标准物质：系指供药品检验（鉴别、检查、含量或效价测定）中使用的，具有确定特性量值，用于校准设备、评价测量方法、给供试药品赋值或者鉴别用的物质。国家药品标准物质共有五类：标准品、对照品、对照药材、对照提取物、参考品。 24. 标准品：系指用于生物检定或效价测定的标准物质，其特性量值按效价单位（U）或重量单位（μg）计，以国际标准物质进行标定，供试品的效价以标准品的效价单位赋值。 25. 对照品：系指采用理化方法进行鉴别、检查或含量测量时使用的标准物质，其特性量值一般按纯度（%）计。📦 贮藏术语考点 26. 避光：系指避免日光直射； 27. 遮光：系指用不透光的容器包装； 28. 密闭：系指可防止尘土及异物进入的容器包装； 29. 密封：系指用可防止风化、吸潮、挥发或异物进入的容器包装； 30. 熔封或严封：系指可防止空气、水分的侵入与微生物污染的容器或适宜的材料包装； 31. 阴凉处：系指贮藏处温度不超过\boldsymbol{20℃}； 32. 凉暗处：系指贮藏处避光且温度不超过\boldsymbol{20℃}； 33. 冷处：系指贮藏处温度为\boldsymbol{2℃～10℃}； 34. 常温：系指温度为\boldsymbol{10℃～30℃}。✅ 四、生物药剂学与药物结构考点 35. 生物等效性研究方法按照研究方法评价效力，其优先顺序为药代动力学研究（评价指标Cmax和AUC）、药效动力学研究、临床研究和体外研究。 36. 血样包括：全血、血浆、血清（血浆：更可靠的指标；血清：制备方便，更常用）。 37. 羟甲戊二酰辅酶A还原酶抑制剂类降血脂药物的药效团：3，5-二羟基羧酸。🔗 药物与作用靶标的结合形式 38. 共价键：是一种不可逆的结合形式，多发生在化学治疗药物的作用机制上，如烷化剂类抗肿瘤药物，对DNA中鸟嘌呤碱基产生共价结合键，产生细胞毒活性。 39. 离子键（盐键）：去甲肾上腺素与β肾上腺素受体、拟胆碱药物氯贝胆碱与M胆碱受体相结合。 40. 氢键：酰胺类利尿药与碳酸酐酶结合、水杨酸甲酯形成分子内氢键，用于肌肉疼痛的治疗。 41. 离子-偶极和偶极-偶极相互作用：通常见于羰基类化合物，如镇痛药美沙酮与阿片受体结合产生镇痛作用。 42. 金属络合物可用作金属中毒时的解毒剂，二巯基丙醇作为锑、砷、汞的螯合解毒剂。 43. 药物与生物大分子的相互作用有时不单纯是一种结合模式，普鲁卡因的结合模式有：范德华力、偶极-偶极作用、静电引力、疏水性作用。🧪 BCS药物分类 44. 第Ⅰ类药物特点：高溶解度、高渗透性的两亲性分子药物，其体内吸收取决于溶出度，代表药物：普萘洛尔、马来酸依那普利、盐酸地尔硫䓬。 45. 第Ⅱ类药物特点：低溶解度、高渗透性的亲脂性分子药物，其体内吸收取决于溶解度，代表药物：双氯芬酸、卡马西平、吡罗昔康。 46. 第Ⅲ类药物特点：高溶解度、低渗透性的水溶性分子药物，其体内吸收取决于药物渗透率，代表药物：雷尼替丁、纳多洛尔、阿替洛尔。 47. 第Ⅳ类药物特点：低溶解度、低渗透性的疏水性分子药物，体内吸收比较困难，代表药物：特非那定、酮洛芬、呋塞米。 48. 酸性药物：\boldsymbol{pK_a=pH+log[HA]/[A^-]} ；碱性药物：\boldsymbol{pK_a=pH+log[HB^+]/[B]}。🧬 官能团对药效的影响 49. 烃基：脂溶性↑、脂水分配系数（logP）↑，位阻↑，稳定性↑。环己巴比妥引入甲基→海索比妥，不易解离。 50. 卤素：有较强的电负性，会产生电性诱导效应，脂溶性↑，改变电子分布。安定作用：氟奋乃静＞奋乃静；抗炎作用：醋酸氟氢化可的松＞醋酸氢化可的松。 51. 羟基：增强与受体结合力，水溶性↑，改变活性。 52. 胺类：①活性：伯胺＞仲胺＞叔胺；②季铵：作用强，水溶性大，不易透过生物膜和血脑屏障，无中枢作用。🌀 对映异构体药效特点 53. 对映异构体之间具有等同的药理活性和强度：普罗帕酮、氟卡尼。 54. 对映异构体之间产生相同的药理活性，但强弱不同：氧氟沙星、氯苯那敏、萘普生。 55. 对映异构体中一个有活性，一个没有活性：L-甲基多巴、氨己烯酸。 56. 对映异构体之间产生相反的活性：哌西那朵、扎考必利、依托唑啉、异丙肾上腺素。 57. 对映异构体之间产生不同类型的药理活性：右丙氧芬—左丙氧芬、麻黄碱—伪麻黄碱、奎宁—奎尼丁。 58. 一种对映体具有药理活性，另一对映体具有毒性作用：氯胺酮、乙胺丁醇、青霉胺、四咪唑、米安色林、左旋多巴。✅ 五、药物代谢、各类药物考点🔄 药物代谢反应 59. 含芳环的药物——氧化代谢：普萘洛尔→羟基普萘洛尔；丙磺舒→无苯环氧化代谢产物；氯丙嗪；保泰松→羟布宗；苯妥英→羟基苯妥英；S-（-）-华法林→7-羟基华法林。 60. 烯烃：环氧化合物→二羟基化合物；例：卡马西平（环氧化物有抗惊厥活性）；己烯雌酚（己烯雌酚环氧化物）。 61. 含饱和碳原子的药物——氧化：地西泮（羰基的α-碳原子羟基化→替马西泮，经N-脱甲基和α-碳原子羟基化→奥沙西泮）。 62. N-氧化反应（叔胺、含氮芳杂环），如吗啡、胍乙啶、氨苯砜。 63. 醚类药物——O-脱烷基化反应。→醇或酚，以及羰基化合物。大部分是芳香醚。例：可待因、吲哚美辛。 64. 亚砜类的代谢：①氧化→砜；②还原→硫醚。例：舒林酸（前药）。 65. 含硝基的药物：芳香族硝基还原→芳香胺，例：氯霉素。 66. 葡萄糖醛酸的结合反应有：O、N、S和C的葡萄糖醛苷化和O、N、S的葡萄糖醛酸酯化、酰胺化。 67. 与谷胱甘肽的结合反应——白消安。 68. 乙酰化结合反应--对氨基水杨酸。 69. 甲基化结合反应--肾上腺素。 70. 抗过敏药物特非那定、阿司咪唑因干扰心肌细胞K⁺通道，引发致死性尖端扭转型室性心动过速，被美国FDA从市场撤回。 71. 奥沙西泮为地西泮的代谢产物，毒性低、副作用小，对焦虑、紧张及失眠均有效。 72. 三唑仑中三氮唑分子中的甲基提高了脂溶性，使其起效快，但甲基易被代谢成羟甲基失活，而成为短效镇静催眠药。 73. 佐匹克隆属于吡咯烷酮类药物，且其主要镇静催眠作用来自其右旋体。 74. 吩噻嗪类药物副作用：①光毒化变态反应（红疹，减少户外活动，避免日光照射）；②锥体外系反应。 75. 帕利哌酮是利培酮的活性代谢物，药用外消旋体。 76. 常用的去甲肾上腺素再摄取抑制剂：丙米嗪、氯米帕明、地昔帕明、阿米替林、多塞平。 77. 常用的选择性5-羟色胺再摄取抑制药有：西酞普兰、氟伏沙明、氟西汀、舍曲林、盐酸帕罗西汀。 78. 常用的单胺氧化酶抑制药有：吗氯贝胺、托洛沙酮。 79. 常用的5-羟色胺与去甲肾上腺素再摄取抑制剂：度洛西汀、文拉法辛、米氮平。 80. 吗氯贝胺与苯甲酰胺舒必利和甲氧氯普胺结构相似，对MAO-A有可逆性抑制作用，从而提高脑内去甲肾上腺素、多巴胺和5-羟色胺的水平，产生抗抑郁作用。 81. 瑞芬太尼分子中存在羧酸酯结构，具有起效快、维持时间短的特点，临床用于诱导和维持全身麻醉期间止痛、插管和手术切口止痛。 82. 烯丙吗啡和纳洛酮临床上可用于服用吗啡或海洛因中毒的成瘾者的解救。 83. 苯海拉明为氨基烷基醚类代表药，能竞争性阻断组胺H₁受体而产生抗组胺作用。 84. 茶苯海明克服了苯海拉明的嗜睡和中枢抑制副作用，临床用于防治晕动症。 85. 氯雷他定强效、长效、选择性对抗外周H1受体的非镇静类H1受体阻断药，地氯雷他定是氯雷他定的活性代谢物，为第三代受体阻断药。 86. 氯苯那敏含有一个手性碳原子，H1受体抗体均为S-（+）-体，临床用外消旋体的马来酸盐。 87. 甲基多巴为前体药物，临床实用外消旋体，用于治疗高血压、适用于肾性高血压和妊娠高血压。 88. 肾上腺素受儿茶酚-O-甲基转移酶（COMT）和单胺氧化酶（MAO）的催化。 89. 贝诺酯是阿司匹林分子中的羧基与对乙酰氨基酚的酚羟基成酯后的药物。 90. 对乙酰氨基酚其主要代谢物是与葡萄糖醛酸或硫酸结合产物，少部分可由CYP450氧化酶系统转化成毒性代谢产物N-羟基衍生物和N-乙酰亚胺醌；乙酰亚胺醌可耗竭肝内储存的谷胱甘肽，引起肝坏死；各种含巯基的药物可用作对乙酰氨基酚过量的解毒剂。对乙酰氨基酚不具有抗炎作用。 （后面剩余200+考点完整收录在资料中，篇幅原因，推文只展示部分核心考点） 91. 舒林酸前体药物，它在体外无效，在体内经肝代谢，甲基亚砜基被还原为甲硫基化合物而显示生物活性。 92. 塞来昔布胃肠道副作用小，但在临床使用中具有潜在心血管事件风险。 93. H2受体阻断药：西咪替丁结构：咪唑+含硫醚四原子链+末端取代胍；盐酸雷尼替丁为反式体，顺式体无活性。 94. 质子泵抑制药：奥美拉唑—前药循环；清除率：R-异构体＞S-异构体；R-异构体经CYP2C19酶催化代谢，S-异构体经CYP3A4途径代谢。 95. 艾司奥美拉唑是第一个上市的光学活性质子泵抑制药。 96. 甲氧氯普胺分子中含苯甲酰胺结构，有锥体外系副作用，常见嗜睡和倦怠。 97. 伊托必利具有阻断多巴胺D2受体活性和抑制乙酰胆碱酯酶活性的双重活性；通过对D2受体的拮抗作用而增加乙酰胆碱的释放，同时通过对乙酰胆碱酯酶的抑制作用来抑制已释放的乙酰胆碱分解，增强胃、十二指肠收缩力，加速胃排空，并有止吐作用。中枢神经系统分布少，选择性高，不良反应少。不产生甲氧氯普胺的锥体外系症状，无西沙必利的致室性心律失常及其他严重的药物不良反应。 98. 血管紧张素转换酶抑制药：依那普利是双羧基ACE抑制剂药物的代表，分子中含三个手性中心，均为S构型，代谢为依那普利拉（只能静注，而依那普利口服好）。 99. 卡托普利是含巯基的ACE抑制剂的唯一代表；巯基和脯氨酸片段：关键药效团；斑丘疹和味觉障碍的高发生率与卡托普利的巯基（-SH）有关。 100. 赖诺普利和卡托普利也是当前唯一使用的两个非前药的ACE抑制剂。 101. 缬沙坦：用于各类轻、中度高血压，尤其对ACE抑制剂不耐受的患者；缬沙坦+氨氯地平，治疗原发性高血压，特别是单药治疗不能充分控制血压的患者；缬沙坦+氢氯噻嗪，治疗单一药物不能充分控制血压的轻度至中度原发性高血压。 102. 羟甲戊二酰辅酶A还原酶抑制药中属于前药的有：洛伐他汀、辛伐他汀；非前药的有：普伐他汀、氟伐他汀、阿托伐他汀、瑞舒伐他汀。 103. 洛伐他汀为天然HMG-CoA还原酶抑制剂，内酯结构（前药），体外无HMG-CoA还原酶抑制作用，水解为3，5-二羟基戊酸才表现出活性，能显著降低LDL水平，并能提高血浆中HDL水平，用于治疗高胆固醇血症和混合型高脂血症，也可用于缺血性脑卒中的防治。 104. 硝苯地平为对称结构的二氢吡啶类药物，无手性碳，用于治疗冠心病，缓解心绞痛，适用于各种类型的高血压。 105. 尼群地平4位碳原子具手性，临床用外消旋体，为选择性作用于血管平滑肌的钙通道阻滞剂，降压作用温和而持久。 106. 氨氯地平2位甲基被2-氨基乙氧基甲基取代，3、5位羧酸酯的结构不同，1个手性碳，临床用外消旋体和左旋体。 107. 尼莫地平容易通过血脑屏障，临床用于预防和治疗蛛网膜下出血后脑血管痉挛所致的缺血性神经障碍、高血压和偏头痛等。 108. 维拉帕米含有手性碳，右旋体作用强，现用外消旋体，化学稳定性好，呈弱酸性，但甲醇溶液紫外线2h可分解50%。代谢：N-脱甲基（去甲维拉帕米）。 109. 地尔硫䓬：有2个手性碳原子，具有四个立体异构体，临床仅用其d-顺式异构体，即（2S，3S）-异构体，较高的首过效应，主要代谢途径为脱乙酰基、N-脱甲基和O-脱甲基化。 110. 华法林钠含有一个手性碳，S-异构体的抗凝活性是R-异构体的4倍，药用其外消旋体，主要经肝脏CYP450酶代谢，故甲硝唑、氯霉素、西咪替丁、奥美拉唑和选择性5-羟色胺再摄取抑制药，可使本品的代谢减慢，半衰期延长，抗凝作用加强。 111. 氯吡格雷一个手性碳原子，为S-构型，体外无活性，前药，临床用于预防缺血性脑卒中、心肌梗死及外周血管病等。 112. 肾上腺糖皮质激素的基本结构是含有\triangle^4-3，20-二酮和11，17α，21-三羟基孕甾烷。📝 备考小结 药一学习切忌死记硬背，优先抓住基础概念、药典贮藏、药物官能团、对映异构体、药物代谢这几大高频板块。 这份300考点笔记，适合一轮复习打底、二轮刷题复盘、考前快速过一遍核心考点。