ADO-Trastuzumab Emtansine

抗体药物偶联物（Antibody-Drug Conjugate, ADC）是一款兼具靶向药物精准定位能力与化疗药物强效杀伤活性的新型治疗药物。它开辟了癌症治疗的全新赛道，也为无数癌症患者带来了新的希望。 01 初识ADC：什么是抗体药物偶联物？ ADC是通过靶向肿瘤特异性抗原的单克隆抗体，将偶联于抗体上的毒性药物精准递送至肿瘤细胞并杀伤肿瘤的靶向治疗药物。 其核心结构由三部分组成：负责识别肿瘤细胞的单克隆抗体（Antibody）、具备细胞毒性的载荷药物（Payload）以及连接两者的连接子（Linker）。 ► 单克隆抗体：精准识别肿瘤细胞表面高表达的特异性抗原。 ► 载荷药物：对肿瘤细胞发挥直接杀伤作用。 ► 连接子：稳定承载并连接抗体与载荷。 ADC的结构 （DOI：10.1007/978-3-031-83005-1） ADC根据摄取机制可分为内吞型和非内吞型两类。 ► 内吞型ADC：抗体与癌细胞表面靶抗原结合后，通过内吞作用进入细胞，在溶酶体中降解后释放细胞毒性载荷，这类ADC依赖癌细胞高表达内吞型抗原，对靶点和抗体的选择要求严苛。 ► 非内吞型ADC：无需依赖细胞内吞与溶酶体降解，而是利用肿瘤微环境与健康组织的理化差异，使连接子在细胞外发生特异性切割并释放载荷，其靶点范围更广泛，但对载荷的扩散性能要求更高。 目前已获批的ADC均为内吞型，非内吞型 ADC仍处于研发或临床试验阶段。 内吞型和非内吞型ADC的作用机制 （DOI：10.1039/D2CS00446A） 02 组件设计：如何设计高效的ADC？ 一款高效 ADC的成功，离不开抗体、连接子、载荷的 “黄金搭配”。三者需具备良好的稳定性与生物相容性，在到达目标部位前不被降解、不提前发挥杀伤作用；同时需拥有合适的偶联位点，确保偶联过程不影响自身结构与功能，以适配后续生产需求。 2.1 理想抗体的必备技能 ADC抗体的性能直接决定靶向精度。理想抗体需具备良好的特异性、稳定性和穿透能力，能够安全到达靶标所在位置并精准发挥作用。 ► 提高特异性：选择疾病特异性的靶点和优化抗体结构。 ► 增强稳定性：使用完整的IgG作为抗体，可以增强抗体的稳定性。完整的IgG在体内不容易被降解，且被非特异性内吞到非目标细胞内时可以结合FcRn受体回到细胞外 ► 增强穿透能力：关键在于控制亲和力。亲和力的理想范围一般在7-23nM。亲和力过高（<1nM）会导致抗体绑定肿瘤外层细胞后快速内化，无法穿透肿瘤组织深层；过低（>200nM）则容易被循环系统清除。 ► 促进内吞（针对内吞型ADC）：需要强效结合促进内吞的靶点并进入溶酶体。在抗体恒定区引入溶酶体识别相关的短肽序列（如Lys-Asp-Glu-Leu），可以直接引导复合物优先分选至溶酶体释放载荷，避免被回收至细胞膜。 2.2 理想连接子的多重考验 连接子分为非可切割连接子和可切割连接子两大类。 ► 非可切割连接子（Noncleavable Linkers）：无主动切割位点，需依赖溶酶体水解酶降解抗体骨架来释放载荷，优点是稳定性极高，缺点是载荷释放效率较低。 ► 可切割连接子（Cleavable Linkers）依赖肿瘤细胞内特有环境主动断裂，释放游离活性载荷。此类连接子载荷释放效率更高，但稳定性稍差。可切割连接子可以分成三类： ① 酸敏感连接子含有在低 pH（4.5-5.0）条件下可被水解的肼键或酯键。 ② 还原敏感连接子含有可被谷胱甘肽等还原剂切断的二硫键。 ③ 肽酶敏感连接子含有可被特定蛋白酶切割的肽序列。 常见的非可切割连接子和可切割连接子的作用机制 （DOI：10.1039/D2CS00446A） 连接子的选择需适配目标环境：内吞型 ADC 的连接子需适配内吞体 / 溶酶体环境（如可被 Cathepsin B 切割的 Val-Cit、Phe-Lys 序列）；非内吞型 ADC 则需适配肿瘤微环境（如可被肿瘤高表达的 MMP 蛋白酶切割的序列）。此外，连接子需不影响抗体与载荷活性，最好可以增强药效，比如通过亲脂性修饰促进载荷扩散（发挥 “旁观者效应” 杀伤邻近癌细胞），或通过 PEG 等亲水性修饰逃避多药耐药，提升载荷滞留效果。 2.3 理想载荷的关键特质 传统ADC载荷主要分为两类：一类是阻断细胞分裂的微管抑制剂（如美登素类DM1、DM4、奥里斯他汀类MMAE、MMAF）；另一类是DNA损伤诱导剂（如卡奇霉素类、PBD二聚体SG3199、喜树碱类SN-38、DXd）。 此外，激活宿主免疫系统的免疫刺激剂（如STING激动剂、TLR激动剂）虽处于研发阶段，但有望成为下一代难治性肿瘤ADC的新型载荷。 理想载荷需具备高毒性（IC50值通常低于10 nM），非内吞型ADC的载荷还需具备强跨细胞膜穿透能力，因此优先选用疏水性载荷。 一些常见的ADC载荷 （DOI：10.3390/cancers16020447） 03 经典案例：T-DM1“诞生记” T-DM1（赫赛莱®/Kadcyla®）是第一批ADC药物，用于HER2阳性乳腺癌治疗，在2008年首次出现在发表文献中，在2019年获批上市，其的研发过程对ADC药物的设计有参考价值。 在抗体与载荷选择上，研发团队选用已临床获批的抗HER2抗体曲妥珠单抗。HER2作为临床验证靶点，胞外域可被抗体精准识别，且曲妥珠单抗的靶向性与安全性已得到临床证实；载荷则锁定美登素衍生物DM1，这款强效抗有丝分裂药物能破坏癌细胞微管结构，阻止细胞分裂，且与曲妥珠单抗搭配可产生协同抗肿瘤效果。 然而，T-DM1的研发之路并非一帆风顺，连接子的优化经历了波折。当时行业内主流的连接子是二硫键可切割连接子SPDP（BA2378）或SPP（BA2428）。然而当时已有研究显示，血液循环中二硫键连接子稳定性不足，脱靶毒性高；而且HER2阳性乳腺癌的内吞体实际为氧化环境，二硫键难以被还原，药物释放不足。最初，研发团队试图在二硫键周围增加甲基取代来提升稳定性，一步步优化连接子结构，却始终未能彻底解决问题。最后，团队直接更改思路，选用了非可切割连接子硫醚连接子SMCC（BA2364），才实现了关键性突破。硫醚连接子SMCC性质稳定，可避免提前释药，且能依赖溶酶体蛋白酶降解抗体释放DM1（BA2321），既保证了疗效，又大幅降低了脱靶毒性，其药代动力学表现远超传统二硫键连接子。 T-DM1面世后不仅为HER2阳性乳腺癌患者带来了新的生存希望，更为后续无数ADC药物的研发照亮了道路。 T-DM1和不同的连接子 （DOI：10.1158/0008-5472.CAN-08-1776） 04 ADC 的未来：精准治疗的“无限可能” 如今，全球已有10余款ADC获批用于癌症治疗，其中TROP2靶向ADC Trodelvy用于三阴性乳腺癌治疗、Nectin-4靶向ADC Padcev用于尿路上皮癌治疗等，均取得了显著临床成效。 此外，ADC的应用场景正从癌症治疗向自身免疫病、感染性疾病延伸，目前已有20余款非肿瘤适应症ADC处于研发阶段。随着抗体工程、连接子技术、载荷设计的不断突破，未来的ADC将更精准、更高效、更安全。 APExBIO一站式供应ADC合成核心物料，涵盖不同类型的连接子和载荷，用专业物料支撑从早期研发到产业化的全流程，助力加速ADC药物研发进程！ ADC载荷  货号 名称（英文） CAS 号 简介 A3631 Monomethyl auristatin E（MMAE） 474645-27-7 奥里斯他汀类微管抑制剂载荷（MMAE） B3270 MMAF 745017-94-1 奥里斯他汀类微管抑制剂载荷（MMAE衍生物） BA2321 DM1 139504-50-0 美登素类微管抑制剂载荷 BA2323 DM4 796073-69-3 美登素类微管抑制剂载荷（DM1衍生物） BA2643 DM21 2243689-80-5 美登素类微管抑制剂载荷（DM1衍生物） C8675 Tub114 2361406-35-9 新型微管抑制剂类载荷 N2133 SN-38 86639-52-3 喜树碱类DNA损伤诱导剂（TOPO I抑制剂） BA1006 卡奇霉素（Calicheamicin） 108212-75-5 经典DNA损伤诱导剂，可破坏DNA双链 BA2320 Dxd 1599440-33-1 喜树碱类DNA损伤诱导剂（TOPO I抑制剂） BA2324 SG3199 1595275-71-0 PBD二聚体类DNA损伤诱导剂，可结合 -左右滑动查看更多- ADC连接子  货号 名称 CAS 号 切割类型 核心功能特征 A9978 Hydroxy-PEG2-(CH2)2-Boc 133803-81-3 非可切割连接子 PEG2链+保护基，提高水溶性 A9979 Hydroxy-PEG4-(CH2)2-Boc 518044-32-1 非可切割连接子 PEG4长链+保护基，延长连接臂 BA2366 MC-Val-Cit-PAB 159857-80-4 可切割-肽酶敏感型 Val-Cit二肽+间隔基 BA2394 Gly-Gly-Phe-Gly-NH-CH2-O-CH2COOH 1599440-20-6 可切割-肽酶敏感型 GGFG四肽序列，蛋白酶识别 BA2403 Fomc-Gly-Gly-Phe-Gly-OH 1817857-75-2 可切割-肽酶敏感型 保护基修饰GGFG四肽 BA2529 Propargyl-PEG5-amine 1589522-46-2 非可切割连接子 炔基+PEG5链，点击化学适配 BA2539 m-PEG11-Amine 854601-60-8 非可切割连接子 长链PEG，提升水溶性 BA2545 Fmoc-NH-PEG5-CH2COOH 635287-26-2 非可切割连接子 Fmoc保护+PEG5链 BA2547 1-Cbz-3-Hydroxyazetidine 1279680-68-0 非可切割连接子 环烷基骨架，增强稳定性 BA2571 Val-Cit 159858-33-0 可切割-肽酶敏感型 Val-Cit二肽可裂解序列 BA2580 Propargyl-PEG2-NHBoc 869310-84-9 非可切割连接子 炔基+PEG2链 + 保护基 BA2587 Fmoc-NH-PEG6-CH2COOH 437655-96-4 非可切割连接子 长链PEG+保护基 BA2613 Fmoc-Gly-Gly-Phe-OtBu 236426-37-2 可切割-肽酶敏感型 保护基修饰GGF三肽 C6575 H-Val-Ala-OH 27493-61-4 可切割-肽酶敏感型 Val-Ala二肽可裂解序列 C8670 Gly-Gly-Phe-Gly（GGFG） 200427-88-9 可切割-肽酶敏感型 四肽蛋白酶识别序列 C8673 Azide-PEG1-Val-Cit-PABC-OH 2055041-40-0 可切割-肽酶敏感型 叠氮+PEG1+Val-Cit BA2379 Fmoc-Val-Cit-PAB 159858-22-7 可切割-肽酶敏感型 Fmoc保护+Val-Cit-PAB序列 C8671 Fmoc-Ala-Ala-Asn(Trt)-OH 1951424-92-2 非可切割连接子 Fmoc+Trt双保护+三肽序列 C8681 4-(4-Acetyl-phenoxy)-butyric acid 65623-82-7 非可切割连接子 乙酰基修饰+羧酸连接位点 BA2364 SMCC 64987-85-5 非可切割连接子 NHS酯+马来酰亚胺，氨基-巯基偶联 BA2367 DBCO-amine 1255942-06-3 非可切割连接子 DBCO基团，无铜点击化学偶联 BA2378 SPDP 68181-17-9 可切割-还原敏感型 吡啶二硫基+NHS酯，二硫键交联 BA2388 sulfo-SPDB 1193111-39-5 可切割-还原敏感型 水溶性二硫基+NHS 酯 BA2402 DBCO-Maleimide 1395786-30-7 非可切割连接子 DBCO+马来酰亚胺，双功能偶联 BA2443 DBCO-PEG4-Maleimide 1480516-75-3 非可切割连接子 DBCO+PEG4+马来酰亚胺 BA2456 Propargyl-PEG2-amine 944561-44-8 非可切割连接子 炔基+PEG2+氨基，双功能偶联 BA2469 DBCO-C6-acid 1425485-72-8 非可切割连接子 DBCO+羧基，点击化学+羧基偶联 BA2485 Mal-PEG1-Val-Cit-PABC-OH 2055041-37-5 可切割-肽酶敏感型 马来酰亚胺+PEG1+Val-Cit C3773 Disuccinimidyl Glutarate(DSG Crosslinker) 79642-50-5 非可切割连接子 双NHS酯，氨基-氨基交联 C8672 DBCO-Val-Cit-PABC-PNP 2994332-18-0 可切割-肽酶敏感型 DBCO+Val-Cit+PNP活性酯 C8674 Azido-PEG1-Val-Cit-PABC-PNP - 可切割-肽酶敏感型 叠氮+PEG1+PNP活性酯 B1003 Mc-Val-Cit-PABC-PNP 159857-81-5 可切割-肽酶敏感型 Mc活性基团+Val-Cit+PABC+PNP活性酯 BA2428 SPP 341498-08-6 可切割-肽酶敏感型 吡啶二硫基+NHS酯，二硫键交联 -自由滑动查看更多- 载荷-连接子偶联物  货号 名称（英文） CAS 号 连接子和载荷 BA2624 CL2A-SN-38 1279680-68-0 连接子：CL2A载荷：SN-38 BA2651 MC-SN38 1473403-87-0 连接子：MC载荷：SN-38 BA2628 SMCC-DM1 1228105-51-8 连接子：SMCC载荷：DM1 BA2676 Val-Ala-PAB-MMAE 1912408-92-4 连接子：Val-Ala-PAB载荷：MMAE BA2680 Ac-Lys-Val-Cit-PABC-MMAE 1650569-89-3 连接子：Ac-Lys-Val-Cit-PABC载荷：MMAE BA2685 MC-EVCit-PAB-MMAE 2873452-49-2 连接子：MC-EVCit-PAB载荷：MMAE BA2705 Azido-PEG4-Val-Cit-PAB-MMAE 1869126-64-6 连接子：Azido-PEG4-Val-Cit-PAB 载荷：MMAE BA2708 Cyclooctyne-O-amido-PEG4-VC-PAB-Gly-Gly-NH-O-CO-Exatecan 2699066-62-9 连接子：Cyclooctyne-O-amido-PEG4-VC-PAB-Gly-Gly-NH-O-CO-载荷：Exatecan BA2711 Val-Ala-PABC-Exatecan 2845164-91-0 连接子：Val-Ala-PABC载荷：Exatecan -左右滑动查看更多- 往期推荐 Cell | 细胞死亡相关小分子——解析RNA Pol II抑制致死机制，助力抗癌研究 Cell | APExBIO助力CD36超规小分子内吞机制验证，重塑药物研发逻辑 聚焦肿瘤治疗研究 | APExBIO化合物库助力细胞程序性死亡的机制探索与抗肿瘤药物开发 互动活动 点击下方卡片参与 FOLLOW US 微信矩阵 服务号 公众号 视频号 产品客服 组学助理 小程序 媒体矩阵 小红书 知乎 哔哩哔哩 抖音 LinkedIn Facebook 关于APExBIO - 滑动查看更多介绍 -         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CHICAGO--(BUSINESS WIRE)--Tempus AI, Inc. (NASDAQ: TEM), a technology company leading the adoption of AI to advance precision medicine, today announced that ten abstracts have been accepted for presentation at the 2025 San Antonio Breast Cancer Symposium (SABCS). The meeting takes place December 9–12 at the Henry B. González Convention Center in San Antonio, Texas. “This year at SABCS, our research highlights the power of multimodal data to help unravel the complexity of breast cancer,” said Ezra Cohen, MD, Chief Medical Officer of Oncology at Tempus. “By integrating genomic, transcriptomic, and real-world clinical data, we are moving beyond broad disease classifications to uncover specific molecular drivers of progression and resistance. These insights are essential for pinpointing patient populations who may benefit from novel therapies and for optimizing treatment strategies to ultimately improve outcomes for those with advanced disease.” Tempus will highlight its latest scientific and clinical research findings via ten poster presentations: Date/Time: Wednesday, December 10, 2025, 12:30 p.m. - 2:30 p.m. CDT Presentation Number: PS1-11-08 Summary: We developed a machine learning model that used clinical, genomic, and transcriptomic features to stratify patients with ER-positive/HER2-negative metastatic breast cancer, based on response to first-line CDK4/6 inhibitor plus endocrine treatment and identify predictors of response. This study demonstrated that multimodal real-world data collected during routine care can provide valuable insights into the biology of response to CDK4/6 inhibitors in patients with metastatic breast cancer and help improve patient stratification. Date/Time: Wednesday, December 10, 2025, 12:30 p.m. - 2:30 p.m. CDT Presentation Number: PS1-11-22 Summary: This study compared transcriptomic and immune profiles in HR+/HER2- metastatic breast cancer across wild-type, PIK3CA-mutant, ESR1-mutant, and co-mutant groups. SFRP2 downregulation was specific to ESR1-mutant tumors, while SCGB2A2 was robustly upregulated in PIK3CA-mutant and co-mutant tumors, suggesting its potential as a diagnostic and therapeutic target. Immune analysis revealed increased M2 macrophages and regulatory T cells in PIK3CA-mutant and co-mutant tumors, with the most pronounced immunosuppressive microenvironment in PIK3CA-mutant cases. Date/Time: Wednesday, December 10, 2025, 12:30 p.m. - 2:30 p.m. CDT Presentation Number: PS1-11-16 Summary: Distinct mutation groups—no-MUT, PIK3CA-MUT, ESR1-MUT, and co-MUT (PIK3CA + ESR1)—exhibited unique clinical and genomic features; co-MUT was linked to more bone metastases, elevated tumor mutational burden, increased polyclonality, and shorter real-world overall survival. Notably, the frequency of ESR1 and co-mutations was higher in patients who underwent late molecular testing, indicating these alterations often emerge after extended endocrine therapy and highlighting the importance of timing in molecular assessment for guiding treatment strategies. Date/Time: Wednesday, December 10, 2025, 5:00 p.m. - 6:30 p.m. CDT Presentation Number: PS2-06-28 Summary: Real-world analysis of male breast cancer revealed broadly similar clinicogenomic profiles between Black and White patients, with HR+/HER2-negative and luminal subtypes predominating. Notable immune microenvironment differences—lower M2 macrophage infiltration and higher PD-L1 negativity in Black patients—may impact immunotherapy response and warrant further research into racial variation. Date/Time: Wednesday, December 10, 2025, 5:00 p.m. - 6:30 p.m. CDT Presentation Number: PS2-08-18 Summary: This study characterized pre-treatment expression of cathepsin proteases prior to T-DXd (cleavable linker) vs. T-DM1 (non-cleavable linker) treatment to understand their impact on clinical outcomes in metastatic breast cancer using the Tempus real-world database. This study demonstrated that among T-DXd treated patients, high cathepsin B and L protease expression was associated with improved outcomes in patients with HR+/HER2- disease, whereas in HER2+ patients, high expression of these proteases was associated with worse survival. In contrast, in the T-DM1 cohort there were no significant associations between protease expression and OS in the overall cohort as well as in the HER2+ cohort. This highlights the potential role of proteases as biomarkers of response to T-DXd in HER2 low/ultralow, but not HER2+ metastatic breast cancer. Date/Time: Wednesday, December 10, 2025, 5:00 p.m. - 6:30 p.m. CDT Presentation Number: PS2-04-11 Summary: This study investigates the impact of first-line and second-line therapy selections on real-world progression-free survival (rwPFS) and real-world overall survival (rwOS) in patients with HR+ HER2- mBC. CDK4/6i significantly outperforms taxane in first-line. Patients who received second-line CDK4/6i following first-line taxane had longer second-line rwPFS than those who received CDK4/6i first-line treatment. The findings suggest that taxane may cause sensitization to CDK4/6i, potentially conferring better survival outcomes in a subset of patients where first-line taxane is advised, or a potential advantage to chemo before CDK4/6i re-challenge. Date/Time: Wednesday, December 10, 2025, 5:00 p.m. - 6:30 p.m. CDT Presentation Number: PS2-06-18 Summary: The study objective was to characterize real-world second-line treatment use and clinical outcomes (rwPFS and rwOS) in a metastatic breast cancer patient population with positive ESR1m test after first-line treatment with AI+CDK4/6i. Findings show that this cohort describes a complex subgroup of patients to treat, with rwPFS outcomes highlighting the need for more effective strategies that address resistance to AI+CDK4/6i and improve patient outcomes. Results from Flatiron Health EHR and Tempus both indicated consistent findings. Date/Time: Thursday, December 11, 2025, 12:30 p.m. - 2:00 p.m. CDT Presentation Number: PS3-12-27 Summary: Tempus Lens was leveraged to assess the Tumor Immune Microenvironment (TIME) across metastatic sites of disease in HR+/HER2- breast cancer compared to TNBC, finding significant differences by site in both subtypes, with HR+/HER2- cancer being less immunogenic overall. Lung, pleura, and peritoneum metastases, along with breast and lymph nodes, showed the highest CD8+ T cell proportions, suggesting a subset of HR+/HER2- patients with these sites may potentially respond to Immune Checkpoint Inhibitor (ICI) therapy. This high variability of TIME profiles across metastatic sites warrants further study in prospective trials to guide patient selection for ICI. Date/Time: Thursday, December 11, 2025, 5:00 p.m. - 6:30 p.m. CDT Presentation Number: PS4-05-21 Summary: Tempus Lens was employed to evaluate the tumor immune microenvironment of HER2+ breast cancer, assessing immune cell infiltration, TMB, PD-L1 status, and HLA allele prevalence, to uncover biomarkers for treatment guidance. A notable percentage of patients with localized and de novo metastatic disease displayed TMB high status and/or PD-L1 positivity. Additionally, TMB-high and PD-L1 positive patients with de novo metastatic disease treated with first-line chemotherapy or anti-HER2 therapy had significantly worse real-world overall survival (rwOS), suggesting a potential therapeutic benefit of incorporating immunotherapy into the treatment paradigm, in both localized and metastatic disease settings. Furthermore, observed ethnic HLA polymorphisms in the cohort may contribute to differences in outcomes and could potentially guide the development of population-specific immunotherapeutic strategies. Date/Time: Friday, December 12, 2025, 12:30 p.m. - 2:00 p.m. CDT Presentation Number: PS5-05-02 Summary: This large multimodal RWD outcome analysis from longitudinal molecular surveillance testing (xF) in HR+/HER2- mBC pts treated with AI+CDK4/6i sheds light on the continuum of ESR1m emergence and patient outcomes from first-line and beyond outside of clinical trial data. Analyses show higher ESR1m incidence is associated with reduced survival regardless of line of therapy. Learn more about Tempus at SABCS 2025 here. About Tempus Tempus is a technology company advancing precision medicine through the practical application of artificial intelligence in healthcare. With one of the world’s largest libraries of multimodal data, and an operating system to make that data accessible and useful, Tempus provides AI-enabled precision medicine solutions to physicians to deliver personalized patient care and in parallel facilitates discovery, development and delivery of optimal therapeutics. The goal is for each patient to benefit from the treatment of others who came before by providing physicians with tools that learn as the company gathers more data. For more information, visit tempus.com. Forward Looking Statements This press release contains forward-looking statements within the meaning of Section 27A of the Securities Act of 1933, as amended (the “Securities Act”), and Section 21E of the Securities Exchange Act of 1934, as amended, about Tempus and Tempus’ industry that involve substantial risks and uncertainties. All statements other than statements of historical facts contained in this press release are forward-looking statements, including, but not limited to, statements regarding the quality of Tempus’ research and publications; the contributions of Tempus’ research and findings to the larger scientific community and the use of Tempus’ products and services to advance clinical care for patients. In some cases, you can identify forward-looking statements because they contain words such as “anticipate,” “believe,” “contemplate,” “continue,” “could,” “estimate,” “expect,” “going to,” “intend,” “may,” “plan,” “potential,” “predict,” “project,” “should,” “target,” “will,” or “would” or the negative of these words or other similar terms or expressions. Tempus cautions you that the foregoing may not include all of the forward-looking statements made in this press release. You should not rely on forward-looking statements as predictions of future events. Tempus has based the forward-looking statements contained in this press release primarily on its current expectations and projections about future events and trends that it believes may affect Tempus’ business, financial condition, results of operations and prospects. These forward-looking statements are subject to risks and uncertainties related to: the intended use of Tempus’ products and services; Tempus’ financial performance; the ability to attract and retain customers and partners; managing Tempus’ growth and future expenses; competition and new market entrants; compliance with new laws, regulations and executive actions, including any evolving regulations in the artificial intelligence space; the ability to maintain, protect and enhance Tempus’ intellectual property; the ability to attract and retain qualified team members and key personnel; the ability to repay or refinance outstanding debt, or to access additional financing; future acquisitions, divestitures or investments; the potential adverse impact of climate change, natural disasters, health epidemics, macroeconomic conditions, and war or other armed conflict, as well as risks, uncertainties, and other factors described in the section titled “Risk Factors” in Tempus’ Annual Report on Form 10-K for the year ended December 31, 2024, filed with the Securities and Exchange Commission (“SEC”) on February 24, 2025, as well as in other filings Tempus may make with the SEC in the future. In addition, any forward-looking statements contained in this press release are based on assumptions that Tempus believes to be reasonable as of this date. Tempus undertakes no obligation to update any forward-looking statements to reflect events or circumstances after the date of this press release or to reflect new information or the occurrence of unanticipated events, except as required by law.