从被嘲“不切实际”到产业热点！药明康德如何助力创新科学走向新药前沿？| Bilingual

十多年前，药明康德收到了一家小型生物技术公司发来的研发需求。读完资料后，相关团队的第一反应是“震撼”。这是他们第一次见到分子量如此之大、结构如此“奇特”的分子。

这种奇特的分子，就是后来引起广泛关注的蛋白降解靶向嵌合体（Proteolysis Targeting Chimera）疗法。

当时，蛋白降解靶向嵌合体和它背后的Arvinas公司，都还没有得到如今的关注。以“诱导接近”（induced proximity）为机理，将致病蛋白“拉近”到细胞里的E3连接酶，针对性地进行靶向蛋白降解，在整个行业里都是一个比较新的概念，少有研发赋能平台接触过这样的化学结构。

为了更好地满足客户的研发需求、助力客户早日实现创新梦想，面对化学上的挑战，药明康德依然毫不犹豫地接受了下来。

这次合作，为药明康德与Arvinas公司往后10年的携手同行拉开了序幕。而蛋白降解靶向嵌合体疗法在临床上取得的进展，也无形之中影响了靶向蛋白降解这一行业浪潮的方向。

“几杯啤酒”聊出来的科学创想

1998年，美国华盛顿州一个风景如画的度假村里，一场学术会议正在召开。

在这里，耶鲁大学的克雷格·克鲁斯（Craig Crews）教授遇到了他的知音——当时在加州理工学院任教的雷蒙德·德沙耶（Raymond Deschaies）教授。他们都非常关注一个研究方向：如何利用细胞天然的“蛋白质回收系统”治疗疾病。

此前已经有科学家发现，细胞内有一种蛋白复合体，它的作用就像“回收站”，可以把异常、废弃的“垃圾蛋白”降解掉。更妙的是，有另外三类酶能通过一系列步骤，给垃圾蛋白“贴上待降解标签”（泛素化处理），这个标签能被“回收站”精准识别，从而降解“垃圾蛋白”。三位科学家因发现这一“泛素介导的蛋白降解系统”，获得了2004年的诺贝尔化学奖。

▲“带标签的垃圾蛋白”（左）被“回收站”（右）识别、降解的过程（图片来源：参考资料[18]）

那天，德沙耶教授正在听克鲁斯教授讲解“如何用小分子把两个蛋白质连在一起”。当时正一心研究泛素连接酶的他，脑中突然闪过一个灵感，问道：如果小分子连接的是蛋白质与泛素连接酶，是不是可以驱动蛋白质的泛素化降解呢？

克鲁斯教授顿时眼前一亮——之前他就想过，很多疾病都有特定的致病蛋白，如果能利用“回收系统”精准降解致病蛋白就好了。而德沙耶教授提出的观点，为他冥思苦想而不得解的难题带来了一条新的解题思路！

顺着这个灵感，两位科学家越聊越投入，一边吃饭，一边还在讨论科学创想。

“几杯啤酒下肚，我们就开始‘异想天开’，然后想到了一条新点子。如果能成功，它将会是一种变革性的新疗法！”

两位科学家的设想是：利用诱导接近机制（通过将蛋白或核酸拉近形成复合体，从而调控靶点功能），让小分子“一只手抓住”（结合）致病蛋白，“另一只手抓住”泛素连接酶，让前者靠近后者并被打上“待降解垃圾”的标签，或许就能利用细胞内的“回收站”降解这些有害蛋白。

▲PROTAC®药物分子设计：一头（左）连上致病蛋白、另一头（右）连接泛素连接酶，后者给前者“贴标签”（图片来源：参考资料[18]）

而且他们敏锐地意识到，相比传统的小分子抑制剂，这种新分子有不同的优势。

传统靶向疗法的思路是，让小分子抑制剂与致病蛋白精准结合，就像一把“钥匙”把致病蛋白的“锁眼”（活性靶点结合位点）反锁起来，让它无法发挥致病作用。问题在于，85%的致病蛋白没有“锁眼”或不容易找到与之吻合的“钥匙”，因此被认为“难以成药/不可成药”；还有一些能“反锁”成功的“钥匙”，由于吻合不够牢固、“锁眼”变异等问题，时间久了也会脱落、失效，即产生了耐药性。

而他们的新方法绕开了“找锁眼配钥匙”的过程，选择直接把“带锁眼的门把手”拆除销毁，让这扇“致病之门”无法打开。因此，那些不可成药和耐药的难题，有望用这种方法直接攻克。

聊了一整个周末，两位科学家一拍即合，很快开始了合作。

2001年，他们开发出了预想中的分子——其一端是与致病蛋白结合的小分子，另一端则与E3泛素连接酶结合的多肽。在实验条件下，研究人员成功展示了它降解致病蛋白质的潜力。

从被嘲“不切实际”到产业热点

起初，这项成果并不被主流科学界看好，因为当时的蛋白降解靶向嵌合体在人体细胞中活性低，远远达不到成药标准，业内大多数人认为它是一种“有趣但不切实际”的实验室工具化合物。根据《自然》杂志2025年的一篇报道，有一些科学家想涉足这一全新的领域，只招来了一些同行的不以为然：“蛋白降解靶向嵌合体？那东西永远成不了药。”

但正所谓“十年窗下无人问，一举成名天下知”，总有一些不被看好的人和事，会随着时间推移爆发出惊人的潜力。

这些年，在无人在意的角落，克鲁斯教授团队顶住压力、一步一个脚印地解决蛋白降解靶向嵌合体的各种硬伤问题，用克鲁斯教授的话说，是在不断“修修补补”。

2008年，他们用小分子替代原本的多肽配体部分，这样整个蛋白降解靶向嵌合体都由小分子模块组成，能提高细胞膜穿透能力和分子的成药性。

2013年，两篇《科学》论文证明，“老药”沙利度胺能清除癌细胞，竟是不经意间利用了靶向蛋白降解机制。而此前，科学家一直没完全弄清楚它的原理。这时人们才意识到，整个方向或许真的可行。这个好消息让克鲁斯教授团队振奋不已：这条路还能走，可能走得通！同年，克鲁斯教授联合创立了专研蛋白降解靶向嵌合体的Arvinas公司。

2015年，多个研究团队在细胞和动物模型中实现了靶蛋白的高效降解，打破了蛋白降解靶向嵌合体“无法成药”的看法，也为产业界注入了信心。一大批专注于蛋白质降解的新兴企业如雨后春笋般涌现出来。如Nurix、Kymera、C4 和PAQ Therapeutics等新锐公司如今均有多款靶向蛋白降解分子处于临床研究阶段；另一方面，多家大型药企也在通过与新锐公司达成合作或启动内部研发项目，布局靶向蛋白降解领域。

与此同时，在解决了口服疗法生物利用度的关键挑战后，靶向蛋白降解药物的研发驶上了快车道，挖掘更多候选蛋白降解靶向嵌合体分子、加快启动临床前研究就成了重中之重。于是出现了开头那一幕——Arvinas公司选择药明康德作为合作伙伴，药明康德不负所托，开启了长达10年的合作之旅。

今日FDA批准了首款蛋白降解靶向嵌合体药物，此时距离首篇蛋白降解靶向嵌合体论文发布已经过去了二十几年。当年风华正茂的一群科学家，如今已两鬓斑白，他们倾注多年心血，逐步解答一道证明题：利用诱导接近机制来靶向蛋白降解，能成药，有治病潜力！

这些研究也让业界逐渐意识到，蛋白降解靶向嵌合体背后的诱导接近机制，其潜力不止于蛋白降解本身。通过“拉近”不同分子之间的相互作用，研究者有望重新设计细胞内的信号网络，并由此催生出更多全新的治疗策略。

从蛋白降解靶向嵌合体到更多创新机制

在蛋白降解靶向嵌合体领域不断突围的同时，克鲁斯教授并未停下脚步，又提出了一种全新的诱导接近技术——调节诱导接近靶向嵌合体（Regulated Induced Proximity Targeting Chimeras），并在2019年创办了专攻这一领域的Halda Therapeutics公司。

调节诱导接近靶向嵌合体并不直接诱导降解，而是“一只手抓住”在癌细胞里高表达的靶点蛋白，“另一只手抓住”细胞赖以生存的关键蛋白。它们构成的三元复合体结构非常稳定，因此癌细胞内的关键蛋白活性会大大受阻，整个细胞也会在药物的影响下逐渐死亡。而健康细胞则由于缺少癌细胞里的靶点蛋白，不会形成复合体，也就不受影响。

▲调节诱导接近靶向嵌合体分子的作用机制（图片来源：参考资料[19]）

鉴于之前成功合作的经验，在成立之初，Halda继续选择与药明康德合作，并在关键新药即将进入临床开发阶段时进一步扩大了与药明康德的合作范畴。

2025年，这家公司公布了其在研药物HLD-0915的1/2期临床试验结果。在研究中，这款靶向雄激素受体的在研疗法表现出令人鼓舞的抗肿瘤活性。2025年年底，强生以总额30.5亿美元完成了对Halda Therapeutics的收购。

2024年药明康德投资者开放日上的报告指出，这两个例子生动地说明了药明康德如何站在产业创新前沿，通过赋能生物技术新锐公司，将突破性的科学研究转化为拯救病患的疗法。

Arvinas时任董事长、总裁兼首席执行官John Houston博士也曾在一次公开访谈中感慨道：“如果没有这种合作关系，我们就不会走到今天的位置。”

近10年来，在“诱导接近”领域，各类创新分子类型也在不断涌现，呈现出百花齐放的态势。

从机制上看，这类疗法主要分为两大类：单价分子胶（molecular glues）与双功能分子（bifunctional molecules），后者既包括蛋白降解靶向嵌合体与调节诱导接近靶向嵌合体分子、化学诱导二聚体（CIDs）、RNA靶向降解分子这些化学小分子，也涵盖双特异性抗体和纳米抗体偶联物这些生物大分子。

诱导接近机制的提出，让药物不再只是抑制或激活某个靶点，而是通过“撮合”两类生物大分子在细胞内相遇，激活天然信号通路，改变蛋白功能或水平。由此，研究者能够通过重塑细胞内蛋白网络，影响过去无法触及的靶点，实现更广泛的治疗可能。

截至目前，全球共有百余款诱导接近疗法正处于积极的临床研究中，靶点涵盖AR、BTK、BCL、EGFR、KRAS、CDK、转录因子IKZF、IRAK等，主要聚焦于肿瘤领域，其次还涉及类风湿性关节炎、特应性皮炎等自身免疫性疾病，痤疮、脂溢性皮炎、慢性自发性荨麻疹等皮肤病，以及慢阻肺、哮喘等呼吸道疾病。其中，多款疗法已进入3期临床阶段，针对多种不同的癌症。随着研发进程的持续推进，这些新疗法未来有望推动诱导接近领域迈入新阶段，为患者带来新的治疗选择。

赋能创新，相互成就，携手共赢

20多年来，以蛋白降解靶向嵌合体与调节诱导接近靶向嵌合体为代表的诱导接近疗法领域，经历了从不被看好到争相布局、从“难以成药”到获得FDA批准上市，这种巨大转变，离不开无数科学家与产业界人士的创新与坚守。

这个故事，也是这些年来新药研发领域飞速发展的一个缩影——曾经“不可成药、难以成药”的靶点，如今有了成药的希望，各类新的治疗模式也展现出治疗复杂疾病的潜力。

尽管这些科学创想在转化为现实疗法的道路上，常会经历各种艰难险阻，但心怀科学梦想的人，无论是创新者还是赋能者，都坚信一件事：在没有路的地方，就去闯出一条路，逢山开路，遇水搭桥。

20多年来，药明康德始终致力于帮助各类规模的创新者降低研发门槛，赋能全球医药创新。去年行业媒体STAT的一篇文章中这样描述药明康德对合作伙伴的助力：药明康德致力于支持全球客户加速研发进程，从小型和新锐生物技术公司（biotech）到大型药企，其CRDMO平台能够“端到端”助力靶向蛋白降解分子从发现、到开发，再到生产交付的全过程。凭借全面综合的能力，药明康德能将有潜力的创新想法高效、高质量地转化为现实。

得益于独特的CRDMO业务模式，药明康德很高兴能在相关疗法领域的发展初期，就为蛋白降解靶向嵌合体和调节诱导接近靶向嵌合体类疗法提供研发赋能，并几乎全程参与产业转化历程。

在一路见证合作伙伴再攀高峰的同时，药明康德也在不断前进，提升自己的赋能能力。在蛋白降解靶向嵌合体刚刚起步时，药明康德前瞻性地布局了相关能力和技术，搭建了集发现、合成、分析纯化和测试等能力于一体的赋能平台，助力全球合作伙伴高效推进药物从早期发现到临床试验阶段；伴随着新型靶向蛋白降解技术的持续涌现，药明康德紧跟科学前沿，迅速构建相关技术平台，如今能力已涵盖蛋白降解靶向嵌合体、调节诱导接近靶向嵌合体、分子胶、自噬靶向嵌合体、溶酶体靶向嵌合体、去泛素化酶靶向嵌合体、核糖核酸酶靶向嵌合体、磷酸化诱导嵌合小分子以及抗体偶联降解剂等主要分子类型。

无论前路是平坦还是崎岖，药明康德都将一如既往，怀着“让天下没有难做的药，难治的病”的愿景，助力创新开拓先锋们奔赴星海征途，守望曙光来临。

The Molecule No One Had Seen Before

How WuXi AppTec Turns Innovative Ideas into Drug Candidates

More than a decade ago, a research request arrived at WuXi AppTec from a small biotechnology company few people had heard of.

The documents described a molecule unlike anything the team had encountered before, large in molecular weight and structurally unconventional. As scientists reviewed the proposal, it became clear they were looking at a type of molecule rarely seen in drug development at the time. The novelty of the structure immediately stood out.

The molecule would later become associated with a growing new direction in drug discovery:Proteolysis Targeting Chimeras, an emerging therapeutic concept that sought to eliminate disease-causing proteins rather than simply inhibit them.

At the time, however, both the technology and the company behind it, Arvinas, remained largely unknown. The concept of employing induced proximity to draw pathogenic proteins into proximity with intracellular E3 ligases, thereby enabling targeted protein degradation (TPD), was still a developing scientific idea, and few R&D enabling platforms had experience working with molecules of such complexity.

Faced with a project that lay outside conventional boundaries, WuXi AppTec chose to move forward, aiming to support the client’s ambitions and explore new scientific territory alongside them.

That decision marked the beginning of a decade-long collaboration between WuXi AppTec and Arvinas, a partnership that would unfold alongside the gradual rise of targeted protein degradation as an important area of drug discovery.

An Idea Born Over “A Few Beers”

The origins of Proteolysis Targeting Chimeras trace back to 1998, at an academic conference in a seaside resort in Washington State.

There, Prof. Craig Crews of Yale University met Raymond Deshaies, then a professor at the California Institute of Technology. Both scientists were captivated by the same question: could the cell’s own protein disposal machinery be harnessed to treat disease?

Inside every cell there exists a sophisticated quality-control system, a molecular recycling center that identifies and destroys damaged or unnecessary proteins. Scientists had discovered that proteins destined for removal are tagged through ubiquitination, enabling cellular machinery to recognize and eliminate them precisely. The discovery later earned three researchers the 2004 Nobel Prize in Chemistry.

During one discussion, Crews described how small molecules might bring two proteins into proximity. Deshaies, deeply engaged in ubiquitin ligase research, saw an unexpected possibility: if a small molecule could link a target protein to a ubiquitin ligase, could it trigger the protein’s destruction?

The idea immediately resonated. Many diseases are driven by pathogenic proteins long considered difficult or impossible to drug. Instead of blocking their activity, perhaps they could be removed entirely.

The conversation continued throughout the weekend.

“After a few beers,” Crews later recalled, “we started thinking wildly—and realized this could become a transformative therapy.”

Their concept relied on induced proximity: one end of a molecule binds a disease protein, while the other recruits an E3 ubiquitin ligase, bringing the two together so the target protein can be labeled and eliminated by the cell’s recycling machinery.

Compared with traditional inhibitors, which function like keys locking a protein’s active site, the approach offers a different strategy.Roughly 85% of disease-related proteins lack suitable binding pockets, making them difficult to target with conventional drugs.Even successful inhibitors often lose effectiveness due to resistance.

Proteolysis Targeting Chimeras proposed bypassing the need for inhibition altogether by removing the protein itself.

By 2001, the researchers demonstrated experimentally that such targeted degradation was possible.

From Skepticism to Momentum

Early reactions from the scientific community were cautious. Initial Proteolysis Targeting Chimeras showed limited cellular activity and fell short of drug-development expectations. A report published in Nature noted that in the early days, many researchers viewed them as intriguing experimental tools rather than viable therapeutics, and skepticism remained widespread.

Progress, however, continued steadily.

Over the following years, Professor Crews’ team refined the technology through what he later described as continuous “tinkering.” A turning point came in 2008, when the entire molecule had a new design, which is close to its current version, improving permeability and drug-like properties.

Momentum grew further in 2013, when two papers published in Science revealed that the anticancer effects of thalidomide relied on targeted protein degradation mechanisms. The findings suggested that the underlying concept might already have clinical precedent. That same year, Crews co-founded Arvinasto translate the approach into therapeutics.

By 2015, multiple research groups demonstrated efficient protein degradation in cellular and animal models, helping shift industry perception. Interest expanded rapidly, and new companies focused on protein degradation began to emerge. Since then, companies such as Nurix Therapeutics, Kymera Therapeutics, C4 Therapeutics, and PAQ Therapeutics have advanced multiple targeted protein degradation molecules into clinical development. Meanwhile, big pharmaceutical companies are actively building pipelines in this area by collaborating with emerging companies or starting internal development.

After key oral bioavailability challenges were addressed at the same time, development accelerated. Arvinas selected WuXi AppTec as a strategic partner to support expanding discovery and preclinical efforts, initiating a collaboration that would extend over the next decade.

Today, more than two decades after Proteolysis Targeting Chimeras were first described in the scientific literature, the FDA approved Veppanu (vepdegestrant), marking the first approval of a drug based on this technology.The pioneers in the field now have gray hair at their temples. They have devoted much of their lives to answering a single question: proving that targeted protein degradation through an induced proximity mechanism can be developed into medicines with the potential to treat disease.

These advances have also prompted the scientific community to recognize that the potential of induced proximity extends beyond protein degradation alone. By bringing different molecules into proximity and reshaping interactions within cellular networks, researchers are beginning to design entirely new therapeutic strategies based on this underlying mechanism.

From Proteolysis Targeting Chimeras to More Innovation

As Proteolysis Targeting Chimeras advanced, Professor Crews continued exploring new scientific directions.

In 2019,he introduced Regulated Induced Proximity Targeting Chimeras, a new modality based on the induced proximity concept, and foundedHalda Therapeutics.

Unlike Proteolysis Targeting Chimeras, these molecules do not induce degradation directly. Instead, they form a ternary complex that selectively disrupts survival pathways in cancer cells: one end binds a tumor-specific protein, while the other engages a protein essential for cell survival. The stable complex impedes the function of the essential protein and thus cause selective cancer cell death.

Healthy cells, on the other hand, remain largely unaffected since they don’t have such a high level of tumor-specific proteins.

Building on earlier collaboration experience, Halda partnered with WuXi AppTec from its founding and later expanded the collaboration as clinical development advanced.

In 2025, Halda reported encouraging antitumor activity signals from a Phase 1/2 trial of its androgen receptor–targeting candidate HLD-0915. In late 2025,Johnson & Johnson completed the acquisition of Halda Therapeutics for $3.05 billion.

Together, these developments illustrated how induced proximity strategies were expanding the boundaries of small-molecule therapeutics.

As noted at the WuXi AppTec 2024 Investor Day, these examples show how WuXi AppTec stands at the innovation forefront, and enables new biotech companies to discover and develop lifesaving medicines from breakthrough sciences.

Former Arvinas CEO Dr. John Houston also reflected: “Without this partnership, we would not be where we are today.”

Over the past decade, within the induced proximity field, a wide variety of innovative molecular modalities have continued to emerge, creating a landscape characterized by remarkable diversity.

Mechanistically, these therapies can be broadly divided into two categories: monovalent molecular glues and bifunctional molecules. The latter include small molecules such as Proteolysis Targeting Chimera and Regulated Induced Proximity Targeting Chimera molecules, Chemically Induced Dimerizers, and RNA-targeting degraders, as well as biologics such as bispecific antibodies and nanobody conjugates.

The concept of induced proximity has fundamentally changed how drugs can work.Instead of merely inhibiting or activating a specific target, these therapies function by “bringing together” two biological macromolecules within cells, thereby activating natural signaling pathways and altering protein function or abundance. By reshaping intracellular protein networks in this way, researchers can influence previously inaccessible targets and unlock broader therapeutic possibilities.

To date, more than 100 induced proximity therapies are currently undergoing active clinical investigation worldwide. Their targets include AR, BTK, BCL, EGFR, KRAS, CDK, transcription factors such as IKZF, and IRAK, among others. Most programs focus on oncology, while others extend into autoimmune diseases such as rheumatoid arthritis and atopic dermatitis; dermatological conditions including acne, seborrheic dermatitis, and chronic spontaneous urticaria; as well as respiratory diseases such as chronic obstructive pulmonary disease and asthma. Several candidates have already advanced into Phase 3 clinical trials across multiple cancer indications. As development continues to progress, these emerging therapies are expected to propel the induced proximity field into a new era, offering patients new treatment options.

Enabling Innovation, Growing Together

Over more than two decades, the field of induced proximity therapies, including Proteolysis Targeting Chimeras and Regulated Induced Proximity Targeting Chimeras, has undergone a remarkable transformation. What was once met with skepticism has become a rapidly expanding area of investment and development. The transformation reflects sustained collaboration between academic innovators and industrial partners working to translate discovery into medicine.

An article published in STAT last year described WuXi AppTec’s role this way: WuXi AppTec supports customers from small and emerging biotechs to large pharmas in advancing their pioneering TPD projects across all stages of its CRDMO platform—from discovery to development and delivery. Its comprehensive capabilities enable the company to help transform promising ideas into reality with speed and quality.

As one of the earliest companies enabling both Proteolysis Targeting Chimera and Regulated Induced Proximity Targeting Chimera programs, WuXi AppTec contributed to bridging foundational science and industrial development through its integrated CRDMO model.

Over time, WuXi AppTec expanded its capabilities alongside the growth of the field itself. Early investments established integrated platforms spanning discovery, synthesis, analytical purification, and testing, enabling partners to advance programs efficiently toward clinical development. As new targeted protein degradation modalities emerged, including molecular glues, Autophagy Targeting Chimeras, Lysosome Targeting Chimeras, Deubiquitinase Targeting Chimeras, Ribonuclease Targeting Chimeras, Phosphorylation Inducing Chimeric Small Molecules, and Degrader Antibody Conjugates, the company continued to broaden its technical infrastructure.

Across laboratories worldwide, molecules emerging from these collaborations are steadily moving closer to patients.

The Road Ahead

Scientific progress rarely follows a straight path. It advances through persistence, collaboration, and a willingness to explore unfamiliar ground.

The story of induced proximity drugs such as Proteolysis Targeting Chimeras and Regulated Induced Proximity Targeting Chimeras reflects decades of inquiry driven by a simple belief: when no path exists, one can be created.

Guided by its vision“Every drug can be made, and every disease can be treated,”WuXi AppTec continues to support innovators pursuing the next generation of therapies, helping translate scientific possibility into tangible medical progress.

Somewhere today, another unfamiliar molecule is being examined for the first time.

And another chapter in drug discovery is beginning.

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