Lovastatin

作者 | 何卫· 编辑 | 陈刚 一颗问世近三十年的蓝色小药丸，被重新端上了顶尖癌症实验室的解剖台。 这一次，它直接瞄向了人类医学最致命的梦魇，癌症转移。 以色列魏茨曼科学研究所（Weizmann Institute of Science）联合美国国家癌症研究所（NCI）抛出了一项重磅研究：西地那非（Sildenafil，俗称“伟哥”/Viagra）能够像一把生锈的铁锁，直接卡死癌细胞内部的胆固醇运输闸门，把癌细胞活活“饿”在原地，阻止它们向全身扩散。 在随后的实验中，当研究团队把伟哥与降脂老药“他汀”联用时，癌细胞连自救的后路都被切断。在对超过4万名男性癌症患者长达20年的真实世界追踪中，同时服用这两种老药的患者，五年死亡风险最高暴降了41%。 美国国家癌症研究所（@theNCI）罕见地在官方账号下场背书。消息一出，整个生物医药圈和硅谷长寿圈彻底沸腾了。 ▲ 美国国家癌症研究所（NCI）官方发文：早期研究表明，西地那非或能通过扰乱肿瘤细胞管理胆固醇的方式，阻止癌症扩散。01.一颗“跨界之王”的第三次意外逆袭 在医药史上，西地那非本来就是个彻头彻尾的“意外之子”。 上世纪90年代初，辉瑞制药的科学家在英国小镇桑威治研发这种化合物时，最初只是想做一款治疗心绞痛的心血管药。结果在威尔士矿工身上做临床试验时，心绞痛没怎么缓解，男受试者们却死活不肯交还剩下的药片。这才成就了后来横扫全球的ED神药“伟哥”；再后来，它又跨界成了治疗肺动脉高压的救命药。 谁也没想到，到了2026年，这颗蓝色药丸迎来了它的“第三世”。 这项发表于美国癌症研究协会（AACR）旗舰期刊《Cancer Research》的研究，由魏茨曼研究所的 Ayelet Erez 教授实验室领衔，合作方名单里不仅有美国国家癌症研究所的 Eytan Ruppin 实验室，还有掌握着数百万人口健康档案的以色列 Clalit 医疗服务机构。 ▲ 发表在《Cancer Research》上的同行评议论文（PMID: 42446922），揭示了 PDE5A 抑制剂限制癌症转移的非经典通路。 他们发现了一个反直觉的机制：伟哥抗击癌症转移，完全脱离了传统已知的“扩张血管、增加血流”功能，靠的是一场发生在癌细胞内部的“物流劫持”。 要理清这场劫持，需要先看癌症如何致命。 绝大多数癌症患者离世，罪魁祸首往往不是原发肿瘤本身，只要肿瘤局限在原地，手术切除和局部放疗大多有应对手段。致命的推手，其实是转移（Metastasis）。 癌细胞要想从原发灶脱落，钻进血管，扛住血液奔流时狂暴的剪切力，再挤进肺部、肝脏或大脑“安家落户”，它必须经历极其剧烈的变形。这就像特种兵空降突袭，身上必须有一套既坚韧又极具弹性的特种装甲。 制造这套装甲的核心建材，正是胆固醇。 我们平时体检看到胆固醇高会害怕，但在微观细胞世界里，胆固醇是细胞膜的“钢筋与润滑油”，也是细胞表面信号收发站（脂筏）的底座。一个准备离家出走、四处侵略的癌细胞，对胆固醇的渴求程度，远远超过安分守己的正常细胞。 而伟哥干的事，就是直接炸毁了癌细胞的胆固醇提货点。02.把仓库门焊死：有粮，却一口也吃不到 细胞里的胆固醇并不是随便乱飘的它们被运进细胞后，会先集中存放在一个叫溶酶体（Lysosome）的“中央回收站”里。 癌细胞要想用这些胆固醇去修补细胞膜、去变形跑路，就必须通过溶酶体大门上的一个专属快递闸机，NPC1转运蛋白，把胆固醇源源不断地运出来。 魏茨曼团队在实验室里看到了极为精妙的一幕：拉响警报 ：当西地那非进入癌细胞，它会干起老本行，抑制 PDE5A 酶，导致细胞内一种叫 cGMP 的信号分子浓度飙升；焊死闸机 ：过去没人知道，飙升的 cGMP 竟然会直接撞上溶酶体大门上的 NPC1 蛋白，并与之死死咬合，像往旋转门里塞进了一根粗铁棍；困死粮草 ：NPC1 闸门一卡死，胆固醇就彻底出不来了。 ▲ 医学专家 Matteo Bassetti 分享的研究机制图解：西地那非提升 cGMP 阻断 NPC1 胆固醇运输蛋白，让癌细胞因缺少胆固醇而难以扩散转移。 在魏茨曼研究所公布的显微镜图像中，经过西地那非处理的乳腺癌组织呈现出一种诡异的画面：代表胆固醇的绿色荧光，密密麻麻地淤积在溶酶体小囊泡里，把仓库撑得快要爆炸；而外面的细胞膜和线粒体，却因为拿不到一丁点胆固醇而陷入瘫痪。 守着满仓黄金，却活活饿死在门外 在医学上，这种现象十分眼熟：罕见遗传病“尼曼-匹克C型病（Niemann-Pick Type C）”患者，正是因为天生 NPC1 基因突变，导致胆固醇滞留在溶酶体中。西地那非的作用，相当于给癌细胞施加了一场精准的“人造遗传代谢病”！ 与此同时，正常细胞由于内部溶酶体回收系统相对稳健，尚能耐受这种扰动；但癌细胞天生溶酶体相关基因表达低下，对这一阻断极为敏感，一旦内部运输受阻，迁移能力便迅速受挫。在小鼠乳腺癌、肺癌、结肠癌模型中，哪怕原发肿瘤体积没有明显缩小，跑到肺部扎根的转移灶数量却出现了断崖式下跌！03.绝杀组合拳：当“伟哥”遇上“他汀” 故事如果只到这里，癌细胞还有机会翻盘。 在演化中活下来的恶性肿瘤，全都是极其狡猾的生存大师。研究团队发现，当溶酶体仓库的大门被伟哥焊死后，饥肠辘辘的癌细胞会立刻拉响内部饥荒警报（激活 SREBP2 通路），启动备用的“地下兵工厂”，既然仓库里的胆固醇拿不出来，那我就自己从头合成！ 怎么破局？答案简单得令人拍案叫绝：再加一颗他汀。 他汀类药物（比如洛伐他汀、阿托伐他汀）是全球数亿中老年人每天都在吃的降血脂基石药物，它的本职工作，恰恰就是砸毁细胞合成胆固醇的“生产线”。西地那非（伟哥） ：焊死溶酶体大门，不准动用库存胆固醇；他汀类药物 ：关停生物合成车间，不准制造新增胆固醇。 两条路同时堵死，癌细胞彻底陷入绝境。实验室数据显示，当洛伐他汀与西地那非联用时，不仅癌细胞的爬行和定植能力被死死按住，大量癌细胞更是直接走向崩溃死亡，而周围的正常细胞几乎毫发无伤。 为了验证这套“双锁机制”在活生生的人体里到底管不管用，研究团队调出了以色列 Clalit 健康数据库的王牌底牌，那里躺着约500万参保者跨越20年的匿名医疗记录。 流行病学家们从中筛选出了 40,567 名在 2008 年至 2017 年间被确诊为癌症的男性患者（年龄在35至65岁之间），并用严格的倾向评分匹配扣除了年龄、吸烟、BMI体重指数和贫富差距的干扰。 最终算出来的五年死亡风险数据，让所有人心头一震： 确诊癌症前开过至少3次西地那非处方的男性，五年死亡风险降低了 26%； 同时使用西地那非 + 他汀类药物的患者，五年死亡风险进一步降低 31%～32%； 而在代谢本就紊乱的 2型糖尿病合并癌症患者亚组中，“伟哥+他汀”组合拳对应的五年死亡风险，更是惊人地降低了 41%！ 这项发现迅速引发了广泛讨论硅谷致力于逆转衰老的知名投资人 Bryan Johnson 第一时间转发了 NCI 的帖文，拆解这套“伟哥+他汀”的双重阻断逻辑，并探讨半衰期更长的同类药“他达拉非（希爱力）”是否也有类似潜力。 ▲ 硅谷长寿网红 Bryan Johnson 转发拆解“伟哥+他汀”阻断癌细胞胆固醇供应的机制，引发广泛讨论。 而在 NCI 官方推文的评论区，网友们则用最美式的黑色幽默消化着这条严肃科学新闻。一条高赞热评只有短短一句话：“抗击癌症，从每一次勃起开始（Fighting cancer, one erection at a time）。” ▲ 网友在 NCI 官方推文下的高赞调侃，让硬核肿瘤学研究破圈传播。04.冷水浇头：横亘在救命药前的“1000倍浓度鸿沟” 看到这里，很多人脑子里一定会冒出一个危险的念头：既然这两样都是药店里几十块钱就能买到的老药，癌症患者是不是明天就可以把伟哥当抗癌药天天吃了？ 千万打住如果盲目照搬，不仅救不了命，反而可能直接送命。 剥开令人振奋的实验室数据和流行病学光环，如果我们用临床药代动力学（PK/PD）的手术刀去剖析这项研究，就会看到一道深不见底的物理壁垒，浓度鸿沟（The Concentration Gap）。 ▲ 科普解析梳理了西地那非阻断 NPC1 的实验机制与观察数据，并明确提醒：现有证据仍停留于临床前与观察阶段，绝不可自行服药抗癌。 让我们算一笔硬核的药理学账： 根据美国 FDA 官方处方指南与经典药代动力学数据，一个成年男性在空腹状态下，吞下一颗常规最高推荐剂量（100毫克）的西地那非后，大约1小时血液浓度达到顶峰。此时，他血液里的西地那非总浓度大约是 1.05 微摩尔（μM）。 表面上看数值似乎接近，但关键门槛在于“血浆蛋白结合率”。 西地那非进入人体血液后，高达 96% 的药物分子会与血浆白蛋白紧密结合。处于结合状态的药物难以自由穿透进入组织细胞发挥作用，游离在外的活性药物仅占约 4%，换算下来，有效峰值浓度仅约 0.042 微摩尔（42 纳摩尔 nM）。 而在魏茨曼研究所的培养皿里，科学家们为了在几十个小时内把癌细胞的胆固醇死死困住，往培养基里倒进去的西地那非浓度是多少呢？通常是 10 到 50 微摩尔（μM） 0.042 微摩尔 vs 10～50 微摩尔。 实验室里用来锁死癌细胞的药物浓度，足足是人体正常服药后游离浓度的 250 倍到 1000 倍以上！ 如果你试图在人体内复刻培养皿里的微摩尔级浓度，一次性吞下几百颗伟哥，会发生什么？遍布全身血管的 PDE5 酶会被瞬间彻底抑制，全身血管极度扩张，血压在几分钟内断崖式崩盘。癌细胞还没来得及饿死，人就已经因为急性顽固性休克和多器官衰竭而死在急诊室里了。更何况，许多中老年肿瘤患者本就合并冠心病，正在服用硝酸甘油等硝酸酯类药物，而伟哥配硝酸甘油，是写进各国药典里的绝对致死禁忌。 此外，伟哥在人体内的半衰期只有短短的 3.8 到 4 小时，吃完几小时就被肝脏代谢干净了；而癌细胞的转移是一场长达数月甚至数年的全天候偷袭。靠偶尔吃一颗短效药脉冲式地“卡一下闸门”，在药理学上很难实现全天候的严密封锁。05.破局启示：老药机制照亮新靶点 这时候，一个极具深度的科学悖论就浮出水面了： 既然正常吃伟哥的血药浓度比实验室低了上百倍，为什么那 40,567 名患者的真实世界数据里，吃伟哥的人死亡率还是实打实地降了 26% 到 41%？ 这正是这项研究最迷人、也最需要审慎推敲的地方。这里有两种截然不同的解释： 第一种可能，是流行病学的“健康使用者偏倚（Healthy User Bias）”。请注意，Clalit 数据库统计的是“确诊癌症前”开过至少三次伟哥处方的男性。在现实生活里，一个五六十岁还依然有活跃性生活需求、愿意主动去看医生开伟哥的男性，他的心血管底子、身体机能、伴侣关系乃至经济条件，大概率本来就比同龄不看男科的病友要好得多。哪怕统计学家用算法校正了吸烟、BMI和收入，这种隐藏在处方背后的“生命力差异”，依然可能美化了生存数据。正如研究共同作者、Clalit 首席流行病学家 Samah Hayek 坦言的那样：这只是确诊前用药的观察性关联，还不能证明确诊后吃伟哥能直接延长寿命，更没有女性患者的数据支撑。 第二种可能，则是慢性微环境蓄积与免疫协同。培养皿里的实验只看几十个小时的急性阻断，需要下猛药；但在人体长达数年的时间跨度里，低剂量的 PDE5 抑制加上他汀的长期配合，或许在肿瘤局部的酸性微环境中产生了慢性蓄积，又或者通过改善肿瘤周围的血管免疫微环境，起到了“四两拨千斤”的慢火熬煮效果。 无论实际机制更偏向哪一种可能，这项研究的核心贡献，在于为防癌转移开辟了新思路。 正如学者 Fulvio Duse（@f_duse）在医学讨论中所指出的：这项发现的价值在于机制启示，理解了这一生物通路，便有望顺藤摸瓜开发出更特异、副作用更小的新型抗转移药物。 ▲ 科学界人士在社交平台上的理性声音：伟哥只是探路石，机制背后的新药研发才是未来。 没错，西地那非只是一把探路的钥匙，它为我们照亮了“cGMP，NPC1，溶酶体胆固醇滞留”这条从未被注意到的暗道。 既然知道了卡死 NPC1 就能饿死转移中的癌细胞，未来的临床药理学家完全有办法绕开“低血压休克”的雷区： 比如，借助纳米脂质体载药系统包裹高浓度西地那非，实现向肿瘤组织的靶向递送与局部释放，降低对全身血管系统的影响； 又比如，以西地那非分子为蓝本进行化学改造，把那个扩张血管的基团剪掉，专门放大它卡死 NPC1 胆固醇闸门的能力，造出亲和力高出几百倍的新一代专属抗转移靶向药。 正如领衔这项研究的 Ayelet Erez 教授所感叹的：“我们必须治疗整个患者，而不仅仅是孤立地看待肿瘤。” 一颗走了三十年弯路的蓝色小药丸，意外撞开了癌细胞最隐秘的后勤仓库大门。它或许还不是那颗能直接终结癌症转移的子弹，但它已经把靶心，清清楚楚地画在了人类医学的准星中央。

Joint recommendation cites Corcept’s CATALYST study on the prevalence and treatment of hypercortisolism in patients whose blood sugar remains high despite use of multiple glucose-lowering medications REDWOOD CITY, Calif.--(BUSINESS WIRE)--Corcept Therapeutics Incorporated (NASDAQ: CORT), a commercial-stage company engaged in the discovery and development of medications to treat severe endocrinologic, oncologic, metabolic and neurologic disorders by modulating the effects of the hormone cortisol, today announced that the American Diabetes Association (ADA) and the European Association for the Study of Diabetes (EASD) published their consensus report on the Management of Type 2 Diabetes, 2026 , which recommends that clinicians screen adults for hypercortisolism if their type 2 diabetes remains difficult to control despite multiple glucose-lowering medications. Citing Corcept’s CATALYST trial, the report notes that cortisol-directed medical therapy with mifepristone reduced HbA1c substantially in such patients and may be beneficial for the management of their hyperglycemia. “Evidence continues to mount that patients whose hyperglycemia does not respond to standard-of-care medications should be screened for hypercortisolism. Excess cortisol can contribute to cardiometabolic disease, including type 2 diabetes and high blood pressure, and cortisol-directed therapy may benefit these patients,” said John B. Buse, MD, PhD, Professor of Medicine, University of North Carolina School of Medicine, and co-chair of the writing group for the ADA/EASD consensus report. Among its consensus recommendations, the report states that “targeted screening for secondary causes of hyperglycemia (e.g., hypercortisolism) should be considered for adults with treatment-resistant type 2 diabetes despite guideline-directed therapy with multiple agents.” The report also advises that, at diagnosis of type 2 diabetes and at regular intervals, hypercortisolism and other alternative diagnoses should be considered based on clinical context and in particular the response of individuals to treatment. In individuals with an HbA1c above 7.5 percent despite multiple glucose-lowering medications and non-ACTH-dependent hypercortisolism, the report states that “cortisol-directed medical therapy with mifepristone reduced HbA1c substantially and may be beneficial for the management of hyperglycemia.” In its discussion of key knowledge gaps, the report observed that “recent studies suggest screening for hypercortisolism identifies a treatable cause in ~25%” and that “developing a better understanding of the role of cortisol-directed therapy in type 2 diabetes is needed.” “There is an urgent need for improved screening for and treatment of hypercortisolism. The findings from our CATALYST study are an important advance in the understanding of this disease. We are heartened that ADA and EASD have recognized this practice-changing research and now recommend that physicians screen patients for hypercortisolism-induced hyperglycemia,” said Bill Guyer, PharmD, Corcept’s Chief Development Officer. The CATALYST trial screened 1,057 patients with difficult-to-control diabetes and found that 24 percent of them had hypercortisolism. The 136 participants with hypercortisolism who proceeded to the trial’s treatment phase were randomized 2:1 to receive either mifepristone or placebo for 24 weeks. HbA1c in patients given mifepristone declined by 1.47 percent, compared to a 0.15 percent reduction in patients given placebo (difference -1.32 percent, p10 percent) were hypokalemia, fatigue, nausea, vomiting, headache, peripheral edema, diarrhea and dizziness. Results from CATALYST were published in Diabetes Care in April and December 2025. Independent experts identified by the two organizations developed the consensus report, which was published simultaneously in Diabetes Care and Diabetologia on October 2, 2026. The full report is available here . The ADA and EASD do not endorse any company or product and were not involved in the preparation of this press release. About Hypercortisolism (Cushing’s syndrome) Hypercortisolism is caused by excessive activity of the hormone cortisol. Symptoms vary, but most patients experience one or more of the following manifestations: hypertension, central obesity, elevated blood sugar and difficult-to-control type 2 diabetes, severe fatigue and weak muscles. Irritability, anxiety, depression and cognitive disturbances are common. Hypercortisolism can affect every organ system and can be fatal if not treated effectively. Cardiovascular events are the most common cause of death. Recent research shows that hypercortisolism is more prevalent than previously believed. In one study 24 percent of patients with difficult-to-control type 2 diabetes were identified as having hypercortisolism. Among patients with both difficult-to-control diabetes and difficult-to-control hypertension, this number increased to 37 percent. About Korlym ® Korlym (mifepristone) modulates the effect of cortisol at the glucocorticoid receptor, one of the two receptors to which cortisol binds, thereby inhibiting the effects of excess cortisol in patients with Cushing’s syndrome. Since 2012, Corcept has made Korlym available as a once-daily oral treatment of hyperglycemia secondary to endogenous Cushing’s syndrome in adult patients with glucose intolerance or diabetes mellitus type 2 who have failed surgery or are not candidates for surgery. Korlym was the first FDA-approved treatment for that illness. Korlym Indication & Usage Korlym (mifepristone) is a cortisol receptor blocker indicated to control hyperglycemia secondary to hypercortisolism in adult patients with endogenous Cushing's syndrome who have type 2 diabetes mellitus or glucose intolerance and have failed surgery or are not candidates for surgery. Limitations of use: Korlym should not be used in the treatment of patients with type 2 diabetes unless it is secondary to Cushing’s syndrome. IMPORTANT SAFETY INFORMATION BOXED WARNING: TERMINATION OF PREGNANCY Mifepristone is a potent antagonist of progesterone and cortisol via the progesterone and glucocorticoid (GR-II) receptors, respectively. The antiprogestational effects will result in the termination of pregnancy. Pregnancy must therefore be excluded before the initiation of treatment with Korlym and prevented during treatment and for one month after stopping treatment by the use of a nonhormonal medically acceptable method of contraception unless the patient has had a surgical sterilization, in which case no additional contraception is needed. Pregnancy must also be excluded if treatment is interrupted for more than 14 days in females of reproductive potential. CONTRAINDICATIONS Pregnancy; patients taking simvastatin or lovastatin and CYP3A substrates with narrow therapeutic ranges; patients receiving systemic corticosteroids for lifesaving purposes; women with a history of unexplained vaginal bleeding or endometrial hyperplasia with atypia or endometrial carcinoma; patients with known hypersensitivity to mifepristone or to any of the product components. WARNINGS AND PRECAUTIONS Adrenal insufficiency: Patients should be closely monitored for signs and symptoms of adrenal insufficiency. See full Prescribing Information for further management instructions. Hypokalemia: Hypokalemia should be corrected prior to treatment and monitored for during treatment. Measure serum potassium 1-2 weeks after starting or increasing the Korlym dose, and periodically thereafter. Mifepristone-induced hypokalemia should be treated with potassium supplementation based on severity. If hypokalemia persists despite potassium supplementation, consider adding mineralocorticoid antagonists. Vaginal bleeding and endometrial changes: Women may experience endometrial thickening or unexpected vaginal bleeding. Use with caution if the patient also has a hemorrhagic disorder or is on anticoagulant therapy. Women who experience vaginal bleeding during treatment should be referred to a gynecologist for further evaluation. QT interval prolongation: Avoid use with QT interval-prolonging drugs, or in patients with potassium channel variants resulting in a long QT interval. Exacerbation/Deterioration of Conditions Treated with Corticosteroids: For medical conditions in which chronic corticosteroid therapy is lifesaving, Korlym is contraindicated. Use of strong CYP3A inhibitors: Concomitant use increases mifepristone plasma levels. Use only when necessary and do not exceed a Korlym dose of 900 mg per day. The labeling contains warnings and precautions for Pneumocystis jiroveci Infection and potential effects of hypercortisolemia. See full Prescribing Information for further management instructions. ADVERSE REACTIONS Most common adverse reactions in Cushing’s syndrome (≥20%): nausea, fatigue, headache, decreased blood potassium, arthralgia, vomiting, peripheral edema, hypertension, dizziness, decreased appetite, and endometrial hypertrophy. DRUG INTERACTIONS Drugs metabolized by CYP3A: Administer drugs that are metabolized by CYP3A at the lowest dose when used with Korlym. CYP3A inhibitors: Caution should be used when Korlym is used with strong CYP3A inhibitors. Use only when necessary, and do not exceed a Korlym dose of 900 mg. CYP3A inducers: Do not use Korlym with CYP3A inducers. Drugs metabolized by CYP2C8/2C9: Use the lowest dose of CYP2C8/2C9 substrates when used with Korlym. Drugs metabolized by CYP2B6: Use of Korlym should be done with caution with bupropion and efavirenz. Hormonal contraceptives: Do not use with Korlym. DOSAGE AND ADMINISTRATION Obtain a negative pregnancy test prior to initiating treatment with Korlym in females of reproductive potential, or if treatment is interrupted for more than 14 days. Administer once daily orally with a meal. The recommended starting dose is 300 mg once daily. Renal impairment: Do not exceed 600 mg once daily. Mild-to-moderate hepatic impairment: Do not exceed 600 mg once daily. Do not use in severe hepatic impairment. Based on clinical response and tolerability, the dose may be increased in 300-mg increments to a maximum of 1200 mg once daily. Do not exceed 20 mg/kg per day. Concomitant use of Korlym with a strong CYP3A inhibitor resulted in a 38% increase in mean plasma concentration of mifepristone. For patients already being treated with a strong CYP3A inhibitor, start with a Korlym dose of 300 mg per day and titrate to a maximum of 900 mg per day if clinically indicated. When a strong CYP3A inhibitor is administered to patients already receiving Korlym, adjust the dose as follows: for patients receiving a daily dose of 600 mg, reduce dose to 300 mg. For patients receiving a daily dose of 900 mg, reduce dose to 600 mg. For patients receiving a daily dose of 1200 mg, reduce dose to 900 mg. Titrate if clinically indicated and do not exceed a Korlym dose of 900 mg in combination with a strong CYP3A inhibitor. USE IN SPECIFIC POPULATIONS Lactation: Mifepristone is present in human milk, however, there are no data on the amount of mifepristone in human milk, the effects on the breastfed infant, or the effects on milk production during long term use of mifepristone. About Corcept Therapeutics For over 25 years, we have focused on cortisol modulation and its potential to treat patients with a wide variety of serious disorders. We have discovered more than 1,000 proprietary selective glucocorticoid receptor antagonists. Our development activities include advanced clinical trials in patients with hypercortisolism, a variety of solid tumors, ALS and liver disease. In 2012, we introduced Korlym ® , the first medication approved by the U.S. Food and Drug Administration for the treatment of patients with endogenous Cushing’s syndrome. In March 2026, we introduced Lifyorli ® as a treatment for patients with platinum-resistant ovarian cancer. Lifyorli is the first selective glucocorticoid receptor antagonist approved for the treatment of any disease. We are headquartered in Redwood City, California. For more information, visit Corcept.com. Forward-Looking Statements Statements in this press release, other than statements of historical fact, are forward-looking statements based on our current plans and expectations and are subject to risks and uncertainties that might cause our actual results to differ materially from any future results expressed or implied by such forward-looking statements. In this press release, forward-looking statements include statements concerning the potential for patients to benefit from cortisol-directed therapy, such as mifepristone. A further description of risks and uncertainties can be found in our SEC filings, which are available at our website and the SEC’s website. These risks and uncertainties include, but are not limited to, those related to our ability to: operate our business; study and develop Korlym, relacorilant, miricorilant, dazucorilant, nenocorilant and our other product candidates; those molecules’ clinical attributes, regulatory approvals, mandates, oversight and other requirements; and the scope and protective power of our intellectual property. We disclaim any intention or duty to update forward-looking statements made in this press release. Contacts Investor inquiries: ir@corcept.com Media inquiries: communications@corcept.com