新一代分子膠有望今年獲批，靶向蛋白降解版圖不斷擴(kuò)展 | Bilingual

編者按：誘導(dǎo)接近（induced proximity）機(jī)制通過將蛋白或核酸拉近形成復(fù)合體，從而調(diào)控靶點功能。基于這一機(jī)制開發(fā)的靶向蛋白降解劑（TPD）已成為新藥研發(fā)的熱點之一。與傳統(tǒng)抑制劑不同，它們無需直接抑制靶蛋白活性，而是通過降解疾病相關(guān)蛋白，有望靶向許多長期被認(rèn)為“不可成藥”的靶點。藥明康德在TPD技術(shù)剛剛起步時，就開始布局相關(guān)能力和技術(shù)，積累了豐富的成功經(jīng)驗，搭建起集發(fā)現(xiàn)、合成、分析純化和測試等能力于一體的一站式賦能平臺。本文將回顧2026年第一季度誘導(dǎo)接近領(lǐng)域的最新進(jìn)展，并介紹藥明康德的一體化CRDMO平臺如何高效解決誘導(dǎo)接近藥物開發(fā)過程中的諸多挑戰(zhàn)。

新一代分子膠有望今年獲批，靶向蛋白降解在神經(jīng)退行性疾病領(lǐng)域獲得概念驗證

今年2月，百時美施貴寶（Bristol Myers Squibb）宣布，美國FDA已受理其在研E3泛素連接酶cereblon（CRBN）調(diào)節(jié)劑（CELMoD）iberdomide聯(lián)合標(biāo)準(zhǔn)治療（daratumumab+地塞米松）用于復(fù)發(fā)或難治性多發(fā)性骨髓瘤（RRMM）的（NDA）。FDA有望在今年8月17日前完成審評。新聞稿指出，iberdomide有望成為首個獲批的CELMoD類藥物。Iberdomide是一種高效的CELMoD類藥物，在結(jié)構(gòu)上與來那度胺（lenalidomide）和泊馬度胺（pomalidomide）相似。與來那度胺或泊馬度胺相比，iberdomide與CRBN的結(jié)合親和力提高約20倍，并可誘導(dǎo)CRBN發(fā)生構(gòu)象改變，從而更高效地募集底物并促進(jìn)Ikaros和Aiolos蛋白的降解。

百時美施貴寶的另一款CELMoD藥物mezigdomide在3期臨床試驗SUCCESSOR-2中也獲得積極結(jié)果。Mezigdomide聯(lián)合carfilzomib和dexamethasone（MeziKd），在RRMM患者中，與單用carfilzomib和dexamethasone（Kd）相比，在無進(jìn)展生存期（PFS）方面顯示出統(tǒng)計學(xué)顯著且具有臨床意義的改善。

百時美施貴寶之外，Monte Rosa Therapeutics公司的分子膠降解劑MRT-2359在1/2期臨床試驗中也獲得。MRT-2359與恩扎盧胺（enzalutamide）聯(lián)用，在既往接受多線治療、攜帶雄激素受體（AR）突變的轉(zhuǎn)移性去勢抵抗性前列腺癌（mCRPC）患者中，達(dá)到100%的疾病控制率（DCR）。

在癌癥領(lǐng)域之外，靶向蛋白降解藥物在神經(jīng)退行性疾病領(lǐng)域也獲得概念驗證。Arvinas在今年3月公布了在研蛋白降解劑ARV-102的。該候選藥物旨在特異性靶向并降解富含亮氨酸重復(fù)序列激酶2（LRRK2），用于治療帕金森病（PD）。研究結(jié)果顯示，在接受治療的PD患者中，ARV-102在所有給藥劑量下均可在第14天實現(xiàn)腦脊液（CSF）中LRRK2水平約50%或以上的降低，并在第28天持續(xù)維持這一降幅。

開發(fā)創(chuàng)新靶向蛋白降解策略，多家新銳完成融資或達(dá)成研發(fā)合作

在2026年第一季度，多家專注于開發(fā)創(chuàng)新蛋白降解策略和誘導(dǎo)接近藥物的新銳完成融資。這些公司力圖開拓具有差異化的靶向蛋白降解方式，并進(jìn)一步擴(kuò)展靶向蛋白降解的靶點范圍。其中，EpiBiologics公司宣布完成1.07億美元的B輪融資。該公司專有的EpiTAC平臺是一種模塊化雙特異性抗體系統(tǒng)，生成的雙特異性抗體的一端與靶點蛋白結(jié)合，另一端與在特定組織中富集的降解受體結(jié)合，從而以組織特異性的方式實現(xiàn)致病性細(xì)胞外蛋白的靶向降解。其在研療法EPI-326是一款能夠在腫瘤組織中降解EGFR的雙特異性抗體，在臨床前研究中已經(jīng)表現(xiàn)出強(qiáng)勁且持久的療效，并具有良好的安全性和藥代動力學(xué)特征，預(yù)計在今年開展首個人體臨床試驗。

Enodia Therapeutics公司在今年年初完成2070萬歐元的種子輪融資。該公司專注于開發(fā)選擇性調(diào)控Sec61轉(zhuǎn)位通道（Sec61 translocon）的藥物。在蛋白質(zhì)合成過程中，分泌蛋白和跨膜蛋白會通過該通道進(jìn)入分泌通路。通過靶向這一機(jī)制，Enodia能夠在疾病發(fā)生的上游階段進(jìn)行干預(yù)，特異性降解潛在致病蛋白，同時不影響關(guān)鍵的生理功能。Enodia公司在今年3月從Kezar Life Sciences收購了其基于Sec61通路的發(fā)現(xiàn)和開發(fā)項目。此次收購將使Enodia能夠進(jìn)一步深入理解Sec61選擇性作用機(jī)制，從而拓展生物學(xué)與轉(zhuǎn)化研究方面的認(rèn)知，并加速推進(jìn)關(guān)鍵臨床里程碑的實現(xiàn)。

Laigo Bio在今年年初完成了1700萬歐元超額認(rèn)購種子輪融資。該公司的SureTACs平臺生成的雙特異性抗體能夠同時與靶點膜蛋白和在細(xì)胞膜上表達(dá)的E3連接酶結(jié)合，從而給細(xì)胞膜蛋白打上泛素“標(biāo)簽”，誘導(dǎo)其被溶酶體降解。

Proxima（原VantAI）公司在1月完成8000萬美元的種子輪融資，基于其人工智能（AI）驅(qū)動的藥物發(fā)現(xiàn)平臺開展新一代誘導(dǎo)接近藥物的發(fā)現(xiàn)與開發(fā)。該公司明確表示將不局限于靶向蛋白降解劑的開發(fā)，而將探索誘導(dǎo)接近機(jī)制更為廣泛的應(yīng)用。

圖片來源：123RF

大型藥企仍然在蛋白降解領(lǐng)域持續(xù)布局。今年年初，強(qiáng)生（Johnson & Johnson）公司與TRIANA Biomedicines達(dá)成研發(fā)合作，共同發(fā)現(xiàn)和開發(fā)針對難以成藥的腫瘤學(xué)靶點的新一代分子膠降解劑。益普生（Ipsen）在1月也與Origami Therapeutics公司達(dá)成研發(fā)協(xié)議，共同開發(fā)治療一種罕見遺傳性神經(jīng)退行性疾病的小分子靶向蛋白降解療法。賽諾菲（Sanofi）在今年2月對格博生物（GluBio Therapeutics）進(jìn)行了3000萬美元，支持其治療鐮狀細(xì)胞病的分子膠降解劑GLB-005和GLB-007的開發(fā)。格博生物授予賽諾菲優(yōu)先談判權(quán)（ROFN），以就潛在的GLB-005和GLB-007開展相關(guān)研究、開發(fā)、生產(chǎn)及商業(yè)化的獨(dú)家許可進(jìn)行談判。

隨著誘導(dǎo)接近機(jī)制不斷拓展至更廣泛的靶點類型和疾病領(lǐng)域，其分子設(shè)計復(fù)雜性與體內(nèi)行為不確定性也顯著提升。從分子膠和雙功能降解劑，到細(xì)胞外或組織特異性降解策略，這類創(chuàng)新分子在跨膜滲透、分布、代謝及暴露-藥效關(guān)系等方面均對研發(fā)體系提出了更高要求。如何在早期階段準(zhǔn)確理解其ADME特征，并在復(fù)雜機(jī)制與臨床轉(zhuǎn)化之間建立清晰關(guān)聯(lián)，正成為推動誘導(dǎo)接近藥物成功開發(fā)的關(guān)鍵。

一體化平臺助力靶向蛋白降解藥物開發(fā)

藥明康德藥物代謝與動力學(xué)部（DMPK）在靶向蛋白降解藥物分析與體內(nèi)行為表征方面具備系統(tǒng)化、前瞻性的研究能力，能夠全面應(yīng)對這類大分子化合物的復(fù)雜ADME/藥代特性挑戰(zhàn)。雙功能性靶向蛋白降解大分子常因分子量高、溶解度低、極性與疏水性區(qū)域共存以及體內(nèi)易發(fā)生多種代謝途徑而給傳統(tǒng)DMPK分析帶來難度。藥明康德DMPK團(tuán)隊基于對靶向蛋白降解技術(shù)本質(zhì)及藥代影響因素的深入理解，構(gòu)建了包括體內(nèi)暴露、穩(wěn)態(tài)分布、清除機(jī)制、代謝途徑與藥效相關(guān)暴露分析的整套策略框架，并通過高靈敏質(zhì)譜分析、同位素標(biāo)記追蹤與體內(nèi)外結(jié)合模型等技術(shù)路線揭示靶向蛋白降解分子體內(nèi)行為規(guī)律。

在具體實施方面，團(tuán)隊針對靶向蛋白降解分子體內(nèi)復(fù)雜代謝路徑開展特定的質(zhì)譜定性/定量方法開發(fā)，結(jié)合體內(nèi)酶動力學(xué)與轉(zhuǎn)運(yùn)機(jī)制研究，準(zhǔn)確識別主要代謝物及消除通路，形成從早期候選篩選到臨床前全面DMPK評估的閉環(huán)服務(wù)。此外，藥明康德DMPK通過整合藥效暴露關(guān)系（PK/PD）與靶點占有率分析，為優(yōu)化劑量策略與降低臨床風(fēng)險提供強(qiáng)有力的數(shù)據(jù)支持。這種從機(jī)制洞察到實驗方法與數(shù)據(jù)解讀的一體化能力，使得藥明康德 DMPK平臺能夠為合作伙伴在復(fù)雜靶向蛋白降解藥物開發(fā)過程中提供高質(zhì)量、高確定性的藥代研究支持，有效提升項目決策效率與研發(fā)成功率。

伴隨著創(chuàng)新靶向蛋白降解技術(shù)的持續(xù)涌現(xiàn)，藥明康德緊跟科學(xué)前沿，迅速構(gòu)建相關(guān)技術(shù)平臺，如今能力已涵蓋PROTAC?、分子膠、AUTAC、LYTAC、DUBTAC、RIBOTAC、PHICS以及DAC等主要分子類型。展望未來，藥明康德將持續(xù)以一體化、端到端的CRDMO賦能平臺，助力全球合作伙伴加速創(chuàng)新藥物的研發(fā)生產(chǎn)進(jìn)程，讓科學(xué)突破更快為患者帶來福祉。

Q1 2026 Review of Induced Proximity Drugs

The induced proximity mechanism regulates target function by bringing proteins or nucleic acids into close proximity to form complexes. Targeted protein degraders (TPDs) developed on this basis have become one of the hottest areas in drug discovery. Unlike traditional inhibitors, TPDs do not need to block target activity directly; instead, they eliminate disease-related proteins, opening opportunities to tackle many proteins once deemed “undruggable.” When TPD technology was still in its infancy, WuXi AppTec started building relevant capabilities. Since then, the company has established a comprehensive, integrated platform encompassing discovery, synthesis, purification, analysis, and testing. This article reviews progress in the induced proximity field in Q1 2026 and highlights how WuXi AppTec’s integrated CRDMO platform helps overcome the unique challenges of developing induced proximity medicines.

Next-Generation Molecular Glues May Gain Approval This Year; Targeted Protein Degradation Achieves Proof-of-Concept in Neurodegenerative Diseases

In February this year, Bristol Myers Squibb announced that theU.S. FDA had accepted the New Drug Application (NDA) for its investigational E3 ubiquitin ligase cereblon (CRBN) modulator (CELMoD) iberdomide in combination with standard therapy (daratumumab + dexamethasone) for the treatment of relapsed or refractory multiple myeloma (RRMM).The FDA is expected to complete its review by August 17 this year. According to the press release, iberdomide may become the first approved CELMoD drug. Iberdomide is a potent CELMoD agent structurally related to lenalidomide and pomalidomide. Compared with these earlier agents, iberdomide exhibits approximately 20-fold higher binding affinity to CRBN and can induce conformational changes in the protein, enabling more efficient substrate recruitment and promoting the degradation of the transcription factors Ikaros and Aiolos.

Another CELMoD drug from Bristol Myers Squibb, mezigdomide, has also delivered positive results in the Phase 3 SUCCESSOR-2 clinical trial. When combined with carfilzomib and dexamethasone (MeziKd), the regimen demonstrated a statistically significant and clinically meaningful improvement in progression-free survival (PFS) in RRMM patients compared with carfilzomib and dexamethasone alone (Kd).

Beyond Bristol Myers Squibb, molecular glue degraders are also progressing across the industry. Monte Rosa Therapeutics reported encouraging results from a Phase 1/2 clinical trial of its molecular glue degrader MRT-2359. In combination with enzalutamide,MRT-2359 achieved a 100% disease control rate (DCR) in heavily pretreated patients with metastatic castration-resistant prostate cancer (mCRPC) harboring androgen receptor (AR) mutations.

Outside oncology, targeted protein degradation has also demonstrated proof-of-concept in neurodegenerative diseases. Arvinas released Phase 1 clinical trial data in March for its investigational protein degrader ARV-102, designed to selectively target and degrade leucine-rich repeat kinase 2 (LRRK2) for the treatment of Parkinson’s disease (PD).The results showed that in treated PD patients, ARV-102 reduced LRRK2 levels in cerebrospinal fluid (CSF) by approximately 50% or more across all dose levels by Day 14, with the reduction maintained through Day 28.

Innovative Targeted Protein Degradation Strategies Drive Financing and R&D Collaborations

In the first quarter of 2026, several emerging companies focused on novel protein degradation strategies and induced proximity therapeutics completed financing rounds.These companies aim to develop differentiated approaches to targeted protein degradation and further expand the range of degradable targets.

Among them, EpiBiologics announced the completion of a $107 million Series B financing. Its proprietaryEpiTAC platform is a modular bispecific antibody system in which one arm binds a target protein while the other engages a degradation receptor enriched in specific tissues, enabling tissue-specific degradation of pathogenic extracellular proteins.Its investigational therapy EPI-326, a bispecific antibody designed to degrade EGFR in tumor tissues, has demonstrated strong and durable efficacy in preclinical studies, along with favorable safety and pharmacokinetic profiles. The company expects to initiate its first human clinical trial later this year.

Enodia Therapeutics completed a €20.7 million seed financing round earlier this year.The company focuses on developing drugs that selectively regulate the Sec61 translocon, a channel through which secreted and transmembrane proteins enter the secretory pathway during protein synthesis.By targeting this mechanism, Enodia aims to intervene at an upstream stage of disease biology, enabling the selective degradation of pathogenic proteins while preserving essential physiological functions. In March, Enodia acquired discovery and development programs based on the Sec61 pathway from Kezar Life Sciences. The acquisition is expected to deepen understanding of the selective mechanisms of Sec61 modulation and accelerate key clinical milestones.

Laigo Bio also completed an oversubscribed €17 million seed financing round earlier this year. ItsSureTACs platform generates bispecific antibodies capable of simultaneously binding target membrane proteins and E3 ligases expressed on the cell membrane, thereby tagging membrane proteins with ubiquitin and inducing lysosomal degradation.

Meanwhile, Proxima completed an $80 million seed financing round in January to advance the discovery and development of next-generation induced proximity therapeutics using its artificial intelligence-driven drug discovery platform.The company has stated that it will not limit its efforts to targeted protein degraders but will explore broader applications of induced proximity mechanisms.

Large pharmaceutical companies continue to expand their presence in the protein degradation field. Earlier this year, Johnson & Johnson entered a research collaboration with TRIANA Biomedicines to discover and develop next-generation molecular glue degraders targeting difficult-to-drug oncology targets. Ipsen also signed a research agreement in January with Origami Therapeutics to develop small-molecule targeted protein degraders for a rare hereditary neurodegenerative disease. In February, Sanofi made a $30 million strategic equity investment in GluBio Therapeutics to support the development of molecular glue degraders GLB-005 and GLB-007 for the treatment of sickle cell disease. GluBio granted Sanofi a right of first negotiation (ROFN) for an exclusive license covering research, development, manufacturing, and commercialization of GLB-005 and GLB-007.

As induced proximity mechanisms expand to broader target classes and disease areas, the complexity of molecular design and the uncertainty of in vivo behavior are increasing. From molecular glues and bifunctional degraders to extracellular or tissue-specific degradation strategies, these innovative molecules present higher demands on drug development systems in areas such as membrane permeability, distribution, metabolism, and exposure–response relationships. Accurately understanding ADME characteristics at an early stage and establishing clear links between complex mechanisms and clinical translation are becoming key to the successful development of induced proximity therapeutics.

Integrated Platform Accelerates the Development of Targeted Protein Degraders

WuXi AppTec DMPK has established a comprehensive evaluation framework specifically designed to address the unique analytical and pharmacokinetic challenges of targeted protein degraders such as bifunctional targeted protein degraders. Owing to their bifunctional structure, high molecular weight, poor solubility, and complex absorption and metabolism behaviors, these molecules often fall outside traditional small-molecule DMPK paradigms. Leveraging a deep mechanistic understanding of event-driven pharmacology and extensive experience with novel modalities, WuXi AppTec DMPK has developed a systematic research strategy integrating physicochemical characterization, in vitro ADME profiling, in vivo pharmacokinetic studies, metabolite identification, and exposure–response analysis to support rational optimization throughout preclinical development.

The platform combines tailored experimental design, advanced bioanalytical workflows, and cross-disciplinary collaboration to accurately characterize key properties such as permeability limitations, high plasma protein binding, metabolic pathways, and linker-related metabolite risks that are critical to the success of bifunctional targeted protein degraders. By integrating in vitro and in vivo data with robust PK/PD interpretation and strategic decision support, WuXi AppTec DMPK helps partners shorten development timelines while improving translational confidence. This end-to-end capability positions WuXi AppTec as a strategic partner for advancing next-generation targeted protein degradation therapies from discovery optimization to clinical development with greater efficiency and predictability.

With the continued emergence of innovative targeted protein degradation technologies, WuXi AppTec remains closely aligned with the scientific frontier and has rapidly built related technology platforms. Today, its capabilities cover major molecular modalities including PROTAC?, molecular glues, AUTAC, LYTAC, DUBTAC, RIBOTAC, PHICS, and DAC. Looking ahead, WuXi AppTec will continue leveraging its integrated, end-to-end CRDMO enabling platform to help global partners accelerate the research, development, and manufacturing of innovative medicines—bringing scientific breakthroughs to patients more quickly.

參考資料：

[1] 賽諾菲對格博生物進(jìn)行3000萬美元戰(zhàn)略股權(quán)投資，推進(jìn)鐮狀細(xì)胞病分子膠降解劑開發(fā). Retrieved February 11, 2026, from https://www.glubiotx.com/news--events/113

[2] AMGEN ACQUIRES DARK BLUE THERAPEUTICS, BOLSTERING ONCOLOGY PIPELINE. Retrieved January 6, 2026 from https://www.prnewswire.com/news-releases/amgen-acquires-dark-blue-therapeutics-bolstering-oncology-pipeline-302652998.html

[3] Revolution Medicines Announces FDA Breakthrough Therapy Designation for Zoldonrasib. Retrieved March 23, 2026, from https://ir.revmed.com/news-releases/news-release-details/revolution-medicines-announces-fda-breakthrough-therapy-1

[4] U.S. Food and Drug Administration Accepts Bristol Myers Squibb's New Drug Application for Iberdomide in Patients with Relapsed or Refractory Multiple Myeloma. Retrieved February 17, 2026 from https://www.businesswire.com/news/home/20260217657186/en/U.S.-Food-and-Drug-Administration-Accepts-Bristol-Myers-Squibbs-New-Drug-Application-for-Iberdomide-in-Patients-with-Relapsed-or-Refractory-Multiple-Myeloma

[5] Monte Rosa Therapeutics Presents Updated Clinical Data from Phase 1/2 Study of MRT-2359 in Combination with Enzalutamide in Heavily Pretreated Metastatic Castration-Resistant Prostate Cancer Patients at ASCO Genitourinary Cancers Symposium (ASCO GU). Retrieved February 24, 2026 from https://www.globenewswire.com/news-release/2026/02/24/3243353/0/en/Monte-Rosa-Therapeutics-Presents-Updated-Clinical-Data-from-Phase-1-2-Study-of-MRT-2359-in-Combination-with-Enzalutamide-in-Heavily-Pretreated-Metastatic-Castration-Resistant-Prost.html

[6] Bristol Myers Squibb Announces Positive Phase 3 Results from the SUCCESSOR-2 Study of Oral Mezigdomide in Relapsed or Refractory Multiple Myeloma. Retrieved March 9, 2026, from https://www.businesswire.com/news/home/20260308945507/en/Bristol-Myers-Squibb-Announces-Positive-Phase-3-Results-from-the-SUCCESSOR-2-Study-of-Oral-Mezigdomide-in-Relapsed-or-Refractory-Multiple-Myeloma

[7] Arvinas Announces Positive Phase 1 Data for ARV-102 Showing Greater Than 50% LRRK2 Degradation in the CSF of Patients with Parkinson’s Disease Treated for 28 Days. Retrieved March 18, 2026 from https://www.globenewswire.com/news-release/2026/03/18/3258013/0/en/Arvinas-Announces-Positive-Phase-1-Data-for-ARV-102-Showing-Greater-Than-50-LRRK2-Degradation-in-the-CSF-of-Patients-with-Parkinson-s-Disease-Treated-for-28-Days.html

[8] Enodia Therapeutics Strengthens Sec61 Portfolio Through Acquisition of Preclinical Assets from Kezar Life Sciences. Retrieved March 12, 2026, from https://www.businesswire.com/news/home/20260312627573/en/Enodia-Therapeutics-Strengthens-Sec61-Portfolio-Through-Acquisition-of-Preclinical-Assets-from-Kezar-Life-Sciences

[9] PAQ Therapeutics Announces Series B Extension, Bringing Total Series B Financing to $77 Million; First Patient Dosed in Phase 1 Trial of PT0511, a Pan-KRAS Degrader. Retrieved March 23, 2026, from https://www.paqtx.com/news/paq-therapeutics-announces-series-b-extension-bringing-total-series-b-financing-to-77-million-first-patient-dosed-in-phase-1-trial-of-pt0511-a-pan-kras-degrader/

[10] EpiBiologics Closes $107M Series B to Advance Pipeline of Novel Bispecific Antibodies to Selectively Degrade Extracellular Protein Targets in Oncology and Immunology. Retrieved January 8, 2026, from https://www.businesswire.com/news/home/20260108480524/en

[11] Proxima Raises $80 Million Led by DCVC to Power the Next Generation of Proximity-Based Medicines. Retrieved March 23, 2026, from https://www.businesswire.com/news/home/20260113074220/en/Proxima-Raises-%2480-Million-Led-by-DCVC-to-Power-the-Next-Generation-of-Proximity-Based-Medicines

[12] Enodia Therapeutics Secures €20.7M to Advance a Small-Molecule Platform for Targeted Protein Degradation Enabled by Proteomics and Machine Learning. Retrieved March 23, 2026, from https://www.businesswire.com/news/home/20260108938000/en/Enodia-Therapeutics-Secures-%E2%82%AC20.7M-to-Advance-a-Small-Molecule-Platform-for-Targeted-Protein-Degradation-Enabled-by-Proteomics-and-Machine-Learning

[13] Laigo Bio completes final close of oversubscribed seed financing of €17 million co-led by Biovance Capital and Kurma Partners to advance oncology and auto-immunity programs. Retrieved March 23, 2026, from https://www.globenewswire.com/news-release/2026/03/23/3260153/0/en/Laigo-Bio-completes-final-close-of-oversubscribed-seed-financing-of-17-million-co-led-by-Biovance-Capital-and-Kurma-Partners-to-advance-oncology-and-auto-immunity-programs.html

[14] Origami Therapeutics Announces Global Collaboration with Ipsen to Advance Protein Degrader Program. Retrieved March 23, 2026, from https://origamitherapeutics.com/origami-therapeutics-announces-global-collaboration-with-ipsen-to-advance-protein-degrader-program/

[15] TRIANA Biomedicines Enters into a Research Collaboration with Johnson & Johnson to Identify Oncology Molecular Glue Degraders. Retrieved March 23, 2026, from https://trianabio.com/press-release-1062026-1-1

[16] Gyre Therapeutics Enters into Agreement to Acquire Cullgen to Gain Targeted Protein Degradation Platform and Pipeline. Retrieved March 23, 2026, from https://www.globenewswire.com/news-release/2026/03/02/3247348/0/en/Gyre-Therapeutics-Enters-into-Agreement-to-Acquire-Cullgen-to-Gain-Targeted-Protein-Degradation-Platform-and-Pipeline.html

免責(zé)聲明：本文僅作信息交流之目的，文中觀點不代表藥明康德立場，亦不代表藥明康德支持或反對文中觀點。本文也不是治療方案推薦。如需獲得治療方案指導(dǎo)，請前往正規(guī)醫(yī)院就診。

版權(quán)說明：歡迎個人轉(zhuǎn)發(fā)至朋友圈，謝絕媒體或機(jī)構(gòu)未經(jīng)授權(quán)以任何形式轉(zhuǎn)載至其他平臺。轉(zhuǎn)載授權(quán)請在「藥明康德」微信公眾號回復(fù)“轉(zhuǎn)載”，獲取轉(zhuǎn)載須知。