预约演示

更新于：2025-05-07

CKB

更新于：2025-05-07

基本信息

别名

B-CK、Brain creatine kinase、CKB

+ [6]

简介

Reversibly catalyzes the transfer of phosphate between ATP and various phosphogens (e.g. creatine phosphate) (PubMed:8186255). Creatine kinase isoenzymes play a central role in energy transduction in tissues with large, fluctuating energy demands, such as skeletal muscle, heart, brain and spermatozoa (Probable). Acts as a key regulator of adaptive thermogenesis as part of the futile creatine cycle: localizes to the mitochondria of thermogenic fat cells and acts by mediating phosphorylation of creatine to initiate a futile cycle of creatine phosphorylation and dephosphorylation (By similarity). During the futile creatine cycle, creatine and N-phosphocreatine are in a futile cycle, which dissipates the high energy charge of N-phosphocreatine as heat without performing any mechanical or chemical work (By similarity).

关联

项与 CKB 相关的药物

Ompenaclid

靶点

CKB x SLC6A8

作用机制

CKB inhibitors [+1]

在研机构

Inspirna, Inc.

原研机构

Inspirna, Inc.

在研适应症

结肠转移性腺癌 [+4]

非在研适应症-

最高研发阶段临床2期

首次获批国家/地区-

首次获批日期1800-01-20

项与 CKB 相关的临床试验

NCT05983367

/ Active, not recruiting临床2期

A Randomized Phase 2 Study of Ompenaclid Versus Placebo in Combination With FOLFIRI Plus Bevacizumab in Patients With Previously Treated RAS Mutant Advanced or Metastatic Colorectal Cancer

The purpose of this study is to measure tumor response to treatment with ompenaclid (RGX-202-01) in patients with previously treated RAS mutant advanced or metastatic CRC. All patients will receive treatment with FOLFIRI and bevacizumab. In addition, patients will be randomized to receive either ompenaclid 3000 mg BID or matching placebo (herein referred to as Study Drug). Each treatment cycle is 28 days in duration.

开始日期2023-10-10

申办/合作机构

Inspirna, Inc.

CTIS2023-503356-27-00

/ Not yet recruiting临床2期

A randomized Phase 2 Study of ompenaclid versus placebo in combination with FOLFIRI plus bevacizumab in patients with previously treated RAS mutant advanced or metastatic colorectal cancer - RGX-202-002

开始日期2023-10-02

申办/合作机构

Inspirna, Inc.

NCT03597581

/ Completed临床1期

A Phase 1 Study of RGX-202-01 (Ompenaclid) , a Small Molecule Inhibitor of the Creatine Transporter SLC6a8, as a Single Agent and as Combination Therapy in Patients With Advanced Gastrointestinal Malignancies With Select Expansion Cohorts

This is a Phase 1 study currently evaluating PO administered ompenaclid in combination with FOLFIRI and bevacizumab in patients with advanced (i.e., locally advanced and unresectable, or metastatic) previously treated colorectal adenocarcinoma. The single agent ompenaclid dose escalation stage and the ompenaclid in combination with FOLFIRI and bevacizumab dose escalation stage of the study has been completed; the expansion stage of ompenaclid in combination with FOLFIRI and bevacizumab is ongoing. In April-24 a protocol amendment added a new dose escalation and expansion stage which will evaluate ompenaclid in combination with FOLFOX and bevacizumab in patients with metastatic CRC. It is anticipated that a total of 30 patients will be enrolled in this new dose escalation and expansion stage of the study.

开始日期2018-06-05

申办/合作机构

Inspirna, Inc.

100 项与 CKB 相关的临床结果

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100 项与 CKB 相关的转化医学

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0 项与 CKB 相关的专利（医药）

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607

项与 CKB 相关的文献（医药）

2025-06-01·Metabolism Open

Celastrol targets CKB-mediated futile creatine cycle in human brown adipocytes thermogenesis

Article

作者: Zhang, Shihu ; Yin, Rui ; Ni, Jingyi ; Hua, Siyu ; Wang, Baicheng ; Wu, Yangyang ; Ji, Chenbo ; Zhang, Xiaoxiao ; Tang, Jinlin ; Liu, Xinyue

Celastrol is widely recognized as one of the most potent anti-obesity agents, and its ability to promote adipocyte thermogenesis is thought to be a key mechanism. However, the precise molecular targets through which celastrol modulates thermogenesis in human adipocytes remain unclear. In this study, we synthesized a celastrol-based small molecular probe and employed a combination of photoaffinity labeling (PAL), click chemistry, and Surface Plasmon Resonance (SPR) to identify its direct binding targets. Our results reveal that celastrol directly interacts with creatine kinase B-type (CKB), leading to an increase in CKB protein stability. This suggests that celastrol modulates the futile creatine cycle within human brown adipocytes, thereby contributing to thermogenesis. Collectively, our findings provide new insights into the molecular mechanisms by which celastrol promotes thermogenesis in human brown adipocytes. Notably, we demonstrated that celastrol targets CKB-mediated futile creatine cycle for the first time. These findings not only deepen our understanding of celastrol's role in weight loss but also provides a potential strategy for obesity treatment.

2025-04-13·Biology of Reproduction

Effect of gestational age and fetal sex on metabolism of creatine by uteri, placentae, and fetuses of pigs

Article

作者: Bazer, Fuller W ; Sah, Nirvay ; Lefevre, Carli M ; Seo, Heewon ; Johnson, Gregory A ; Stenhouse, Claire ; Moses, Robyn M ; Wu, Guoyao ; Cain, Joe W ; Halloran, Katherine M ; Newton, Makenzie G

AbstractThe creatine (Cr) biosynthesis pathway buffers adenosine triphosphate in metabolically active tissues. We investigated whether sex of fetus and day of gestation influence Cr in endometrial and conceptus tissues from gilts on days 60 and 90 (n = 6 gilts/day) of gestation. Uterine and conceptus tissues associated with one male and one female fetus from each gilt were analyzed for creatine, messenger RNAs (mRNAs), and proteins for Cr biosynthesis. Total Cr decreased in amniotic fluid but increased in allantoic fluid between days 60 and 90 of gestation for male (P < 0.05) but not for female fetuses (P > 0.05). Endometrial expression of creatine kinase, muscle (CKM), creatine kinase mitochondrial type 1 (CKMT1), and solute carrier family 6, member 8 (SLC6A8) mRNAs increased (P < 0.05) between days 60 and 90 only for female fetuses. On day 60, expression of creatine kinase, brain (CKB) and CKMT1 mRNAs was greater (P < 0.05) for placentae of female than male fetuses. Livers of male fetuses had greater expression of arginine:glycine amidinotransferase (AGAT) and CKB than for females on day 60, while kidneys of female fetuses had greater expression of guanidinoacetate-N-methyltransferase (GAMT) than male fetuses on day 90 (P < 0.05). Localization of GAMT, CKB, CKMT1, and SLC6A8 proteins to uterine and chorionic epithelium was not influenced by gestational age or fetal sex. Arginine-glycine amidinotransferase localized to fetal kidneys and appeared greater on day 90 than on day 60 in both sexes. Thus, expression of the creatine–creatine kinase–phosphocreatine system at the uterine–conceptus interface is affected by gestational age and fetal sex to influence energy homeostasis in pigs.

2025-02-01·Neurochemical Research

Exploring α-synuclein Interaction Partners and their Potential Clinical Implications for Parkinson’s Disease

Article

作者: Sun, Lili ; Ding, Wenyong ; Chen, Yingfei ; Zhang, Wenli ; Gu, Yanan ; Wang, Cui ; Cao, Can ; Ma, Li ; Zheng, Qiuying

Alpha-synuclein aggregates are strongly associated with Parkinson's disease (PD), a degenerative neurological disorder characterized by a progressive loss in motor functions. Our study aimed to unravel the potential interaction partners of α-synuclein for exploring the synucleinpathy of PD related to α-synuclein aggregates. α-synuclein was expressed in E.coli and purified by affinity chromatography followed by isolation and identification of its interaction partners using pulldown assay coupled with LC-MS/MS. The impacts of the identified interaction partners on PD were evaluated based on GSE205450 dataset. Consequently, 157 proteins were identified by the criteria of unique peptide = 5. Four proteins including ACO2, ANT1, ATP5F1B and CKB were confirmed using immunostaining coupled with α-synuclein-pulldown assay. Transcriptomics assay showed that the dominant biological processes influenced by α-synuclein interaction partners with differential expression were energy metabolism. Together with GSE205450, Western blot assay showed that α-synuclein interaction partners involved in energy metabolism were down-regulated in PD patients and the MPTP-lesioned mice. ROC curves indicated their clinical implications as diagnostic indices of PD. Using ANT1 as an example, we found that protein aggregates formed by ANT1 and α-synuclein predominantly solely appeared in the cells and mice with PD-like variations. Thereby, low levels of the interaction partners of α-synuclein associated with energy metabolism were associated with PD pathogenesis via forming protein aggregates. This study provides an insight into developing innovative targets on PD based on synucleinpathy.

项与 CKB 相关的新闻（医药）

2024-08-07

·生物探索

Cell Metab | 吕志民团队阐述Warburg效应通过乳酰化调控DNA损伤修复的机制

引言一个世纪之前，德国生物化学学家Otto Warburg发现肿瘤细胞即使是在氧气充足情况下，优先选择通过糖酵解而不是三羧酸循环获取能量，即Warburg效应。Warburg效应产生的机制是肿瘤细胞显著增加葡萄糖摄取和乳酸生成，同时抑制线粒体中的丙酮酸代谢。乳酸作为重要的能量来源、主要的糖异生前体和信号分子，对多种细胞功能至关重要。此外，乳酸还可作为乳酰基供体用于蛋白质乳酰化，从而调节关键的细胞活动。在糖酵解过程中，乳酸产生于丙酮酸，而丙酮酸激酶M2（PKM2）作为丙酮酸生成酶，在四聚体状态下活性较高，能够将磷酸烯醇丙酮酸（PEP）和ADP转化为丙酮酸和ATP，并在肿瘤细胞中高度表达。 2024年8月6日，浙江大学转化医学研究院/浙江大学医学院附属第一医院/国家基础科学中心/浙江大学基础交叉研究院吕志民教授团队在Cell Metabolism上在线发表了题为Lactylation: Linking the Warburg effect to DNA damage repair的重要评述，阐述了Warburg效应通过乳酰化调控DNA损伤修复的关键机制。吕志民教授先后在Nature、Cell等杂志发表了多篇论文，揭示了Warburg效应及PKM2调控肿瘤发生发展的重要机制，包括发现在受体酪氨酸激酶激活的条件下，PKM2可以进入细胞核内磷酸化组蛋白H3，并诱导β-catenin介导的c-Myc表达，进而增加LDHA表达以促进乳酸生成，最终促进Warburg效应的产生和肿瘤进展（Nature，2011；Cell, 2012）。然而，Warburg效应及PKM2是否在在胶质母细胞瘤（GBM）中参与DNA损伤修复过程，并介导化疗抵抗和肿瘤进展尚不清楚。北京天坛医院张伟教授和江涛院士在同期的 Cell Metabolism 杂志上发表了题为Glycometabolic reprogramming-induced XRCC1 lactylation confers therapeutic resistance in ALDH1A3-overexpressing glioblastoma的研究论文。吕志民教授应邀对这一发现做了重要总结与评述。醛脱氢酶1家族成员A3（ALDH1A3）是胶质母细胞瘤（GBM）细胞中最常见的ALDH同工酶，负责将醛氧化成羧酸，该研究揭示了ALDH1A3非代谢依赖的新功能，即其与PKM2相互作用并促进PKM2四聚体的形成，进而促进胶质母细胞瘤干细胞中乳酸积累，并促进DNA修复蛋白XRCC1的乳酰化修饰及入核，最终促进DNA修复和肿瘤进展。研究还筛选鉴定了一个可以打破ALDH1A3与PKM2相互作用的小分子化合物D34-919，其与化疗药物TMZ联用可以显著增强其抗肿瘤效果（图1）。该评述指出，Warburg效应不仅仅是一个代谢现象，其对多种非代谢细胞活动具有关键影响。糖酵解中的代谢酶和代谢物往往具有“多重功能”，可以通过代谢以及非代谢依赖的方式改变肿瘤细胞的各种重要活动。Warburg效应在肿瘤细胞中与线粒体功能、基因转录、细胞周期和免疫逃逸等过程紧密相连。本研究揭示了非糖酵解酶ALDH1A3与PKM2的相互作用增强糖酵解和乳酸生成的机制，并展示了Warburg效应通过乳酸介导的蛋白乳酰化调控DNA损伤修复的全新发现。干预这一过程在提高胶质母细胞瘤对DNA损伤诱导疗法的敏感性方面具有令人期待的潜力。模式图（Credit: Cell Metabolism）肿瘤中的大量基因突变以及特有的微环境往往会导致代谢酶原有的功能改变，并赋予其新的非代谢酶功能。吕志民团队先后发现代谢酶PKM2 （Nature, 2011, PMID: 22056988; Cell，2012, PMID: 22901803; Molecular Cell, 2014, PMID: 24316223）、PGK1（Molecular Cell，2016, 2017, 2019, PMID: 26942675, 28238651, 31492635）、KHK-A（Nature Cell Biology, 2016, PMID:2708854; Science Advances, 2019, PMID: 31032410）、PCK1（Nature, 2020, PMID: 32322062）、CHKα（Molecular Cell，2021，PMID: 34077757）、HK2（Cell Metabolism, 2022, PMID: 36007522）、CKB（Nature Cell Biology, 2023, PMID: 37156912）和PFKL（Nature Metabolism, 2024, PMID: 38773347）的蛋白激酶活性在肿瘤发生发展中发挥重要作用。这些成果对于全面系统认知肿瘤代谢具有开创性的理论意义。参考文献 https://doi.org/10.1016/j.cmet.2024.06.015 https://doi.org/10.1016/j.cmet.2024.07.011 责编|探索君排版|探索君文章来源|“BioArt” End 往期精选围观一文读透细胞死亡(Cell Death) | 24年Cell重磅综述（长文收藏版）热文 Cell | 是什么决定了细胞的大小？热文 Nature | 2024年值得关注的七项技术热文 Nature | 自身免疫性疾病能被治愈吗？科学家们终于看到了希望热文 CRISPR技术进化史 | 24年Cell综述

2024-05-02

·精准药物

Cancer Cell丨铁死亡在癌症中的作用

癌症是人类主要致死原因之一，因此，不断探索肿瘤学领域的创新治疗方法显得尤为重要。尽管传统治疗方式能够诱导细胞通过凋亡等常规途径死亡，但很多恶性肿瘤对此类治疗显示出了抵抗性，这促使科研人员探索诱导替代性细胞死亡的治疗策略。铁死亡是一种独特的依赖铁的调节性细胞死亡，由细胞膜上过量的脂质过氧化物积累诱导。铁死亡的调节依赖于促铁死亡细胞活动产生的脂质过氧化物与铁死亡防御系统之间的微妙平衡。当促铁死亡活动压倒铁死亡防御机制时，细胞膜上过量的脂质过氧化物积累可以破坏膜完整性，最终触发癌细胞铁死亡，导致肿瘤抑制。反之，癌细胞中铁死亡防御机制上调导致肿瘤进展和转移（图1）。2024年4月8日，MD安德森癌症中心甘波谊教授团队（雷光博士为第一作者，甘波谊教授为通讯作者）在Cancer Cell上发表了题为The roles of ferroptosis in cancer: tumor suppression, influence on the tumor microenvironment, and therapeutic interventions的综述文章，深入论述了铁死亡在肿瘤抑制中的贡献，探讨了铁死亡在肿瘤微环境中的复杂作用，并分析了如何在癌症治疗中靶向铁死亡。图11.铁死亡在肿瘤抑制中的作用日益增长的证据支持铁死亡作为一种天然的肿瘤抑制机制，通过与各种抑癌基因的相互作用发挥其抑制肿瘤的效果（例如p53、BAP1、AMER1、KEAP1、ARF、MLL4等）。此外，特定的致癌突变似乎赋予癌细胞在逃避铁死亡方面的独特优势（例如RAS家族、RBMS1、OTUB1、ACTL6A、CKB、ENO1、PI3K通路、FLT3等）。此外，癌症的淋巴转移过程以及由癌干细胞（CSCs）驱动的肿瘤进展与铁死亡的抑制密切相关（图2）。图22.铁死亡在肿瘤微环境中的作用肿瘤微环境（TME）是由肿瘤细胞、免疫细胞、基质细胞以及其他细胞组成的多方面生态系统。这些组成部分不仅共存，而且还进行复杂的相互作用，显著影响肿瘤的生长和进展。铁死亡与TME以复杂的方式相联系。一方面，癌细胞中的铁死亡可能引发或调节TME中的免疫反应。另一方面，TME中免疫细胞对铁死亡的敏感性差异显著，并且不同类型的免疫细胞可以增强或抑制癌细胞中的铁死亡（图3）。（1）铁死亡癌细胞在接受铁死亡诱导剂（FIN）处理的早期阶段释放多种免疫刺激信号，这些是免疫原性细胞死亡的标志。这些信号促进树突状细胞成熟和巨噬细胞吞噬铁死亡癌细胞的效率，有助于M1型巨噬细胞极化和T细胞在肿瘤中的活动，甚至激活抗肿瘤免疫反应。相反，抑制铁死亡可能减弱T细胞介导的抗肿瘤作用。然而，铁死亡对树突状细胞的影响可能取决于铁死亡的阶段。总之，铁死亡癌细胞对免疫原性的影响似乎取决于具体环境，这使其成为铁死亡研究中有争议的话题。（2） TME组分对铁死亡的调控：TME内不同细胞组分对癌细胞的铁死亡敏感性有着显著影响。CD8+ T细胞通过分泌IFNγ，通过双重机制促进铁死亡：一是抑制SLC7A11表达限制胱氨酸摄取，二是增加ACSL4表达促进PUFA-PL合成。此外，中性粒细胞通过传递含髓过氧化物酶的颗粒诱导癌细胞铁死亡。肿瘤相关成纤维细胞（CAFs）通过上调DLEU1或分泌miR-522抑制癌细胞铁死亡。不同的细胞因子如TGFβ1和IL-1β分别能促进或抑制铁死亡，显示出TME中各组分在铁死亡调控中的复杂作用。这些相互作用不仅影响癌细胞的铁死亡反应，也对抗肿瘤免疫策略的效果产生影响，突显了在未来研究中需要综合利用TME的潜能来促进或克服铁死亡的重要性。（3）铁死亡与先天免疫系统：TME中肿瘤相关巨噬细胞（TAMs）主要表现为免疫抑制的M2表型，但其对铁死亡敏感，而M1型TAMs对铁死亡抵抗。铁死亡诱导疗法的潜力在于可能选择性地靶向并消除M2型TAMs而不影响M1型TAMs，这为改善免疫抑制性TME和提高免疫治疗的效果提供了策略。然而，也有研究显示铁死亡与TAMs之间存在更复杂的相互作用。此外，髓源抑制性细胞（MDSCs）似乎表现出对抗铁死亡或者对铁死亡易感的特性，这取决于具体情况；而肿瘤浸润性中性粒细胞具有高水平的ACOD1，表现出对铁死亡的抗性。最后NK细胞在TME中的功能障碍与脂质过氧化引起的氧化应激有关，铁死亡抑制剂可以增加NK细胞在肿瘤中的存活。总之，这些研究揭示了铁死亡对TME中多种先天免疫细胞类型的复杂影响，深入理解对完善和扩展癌症免疫治疗策略至关重要。（4）铁死亡与适应性免疫系统：铁死亡对适应性免疫系统的影响呈现双刃剑特性。铁死亡可通过如脂质过氧化物等癌细胞释放的产物影响适应性免疫细胞识别肿瘤抗原的能力。GPX4对于维持B细胞的抗体反应和功能至关重要，并且B细胞对GPX4缺失诱导的铁死亡敏感。T细胞对铁死亡的敏感性仍有争议。有研究表明T细胞对铁死亡具有相对的抵抗性，这支持了在不显著损害T细胞介导的抗肿瘤免疫的情况下，可以选择性地在癌细胞中诱导铁死亡。然而，也有研究发现T细胞对GPX4抑制诱导的铁死亡敏感，尤其是CD8+ T细胞。此外，针对调节性T细胞（Treg）的GPX4抑制可以增强抗肿瘤免疫反应，而对滤泡辅助T（TFH）细胞的GPX4抑制则损害抗肿瘤免疫。这些发现强调了铁死亡对适应性免疫细胞的复杂影响，指出了铁死亡调控在增强抗肿瘤免疫策略中的潜力和挑战。图33.在癌症治疗中靶向铁死亡（1）靶向癌细胞对铁死亡的脆弱性：靶向癌细胞中铁死亡的脆弱性是一种引人注目的策略，特别是对于克服某些耐药性癌症。这种方法旨在通过利用癌细胞对铁死亡的增强敏感性来选择性地消除癌细胞，同时保护正常细胞，从而提高治疗效果并最小化不良反应。某些抑癌基因缺失或者致癌突变使癌细胞对铁死亡更加敏感，主要通过重新编程脂质代谢实现。例如，肿瘤抑制基因视网膜母细胞瘤1（RB1）缺失导致了ACSL4介导的PUFA-PL合成增加，使癌细胞对铁死亡敏感。类似地，非小细胞肺癌细胞中的表皮生长因子受体（EGFR）突变导致它们高度依赖于半胱氨酸，使这些细胞对通过SLC7A11抑制或胱氨酸剥夺诱导的铁死亡敏感。此外，特定癌症细胞的代谢特征，如间充质型癌细胞和耐药性癌细胞，使它们对铁死亡特别脆弱，为治疗这些特别棘手的恶性肿瘤提供了有希望的治疗方法。（2）在免疫治疗中靶向铁死亡：在免疫治疗中靶向铁死亡的潜力同样引人注目。例如，结合使用抗PD-L1疗法与半胱氨酸酶或花生四烯酸处理，显著增强了抗肿瘤免疫力。此外，间歇性饮食限制蛋氨酸可通过促进铁死亡使肿瘤对抗PD-1疗法更加敏感，而GPX4抑制剂N6F11可以特异性的在癌细胞中触发GPX4降解，增强了肿瘤对免疫疗法的敏感性。值得注意的是，铁死亡调节因子，如SLC7A11、GPX4或ACSL4，可以作为预测免疫治疗临床结果改善的潜在生物标志物。（3）靶向铁死亡克服治疗抵抗：诱导铁死亡的方法已证明在克服对标准治疗，包括各种靶向治疗、化疗和放疗的抗药性方面是有效的。例如，通过MT1G抑制剂、SLC7A11抑制剂、或者LCN2抗体增强铁死亡可以克服肝癌或肾癌细胞对索拉非尼的抵抗。CDK1抑制剂通过铁死亡依赖机制改善结肠癌中的奥沙利铂抗性，而SLC7A11或GPX4抑制剂可以对抗获得性放射抵抗癌细胞中SLC7A11或GPX4的上调，从而克服放射抵抗。此外，雌激素受体拮抗剂富维司群通过阻碍MBOAT1介导的MUFA-PL合成，使抗激素治疗抵抗的ER阳性乳腺癌对铁死亡脆弱。4.总结与展望近年来，铁死亡作为肿瘤抑制机制及耐药性癌症的潜在弱点，引起了癌症研究的广泛关注。通过靶向调节铁死亡，有望增强免疫治疗的效果，克服传统癌症治疗的抗性。然而，要充分利用铁死亡诱导的治疗潜力，可以进一步探索铁死亡与饮食干预在癌症治疗中的作用，并充分理解铁死亡在不同细胞类型中的复杂性，以及在抗肿瘤免疫中的双重作用。将靶向铁死亡的治疗策略推向临床实践是一项挑战，需要通过严格的临床试验验证FINs的效果，同时识别对铁死亡敏感的患者群体，并开发能够预测和监测对FINs反应的生物标志物。这要求采用集成单细胞组学、空间转录组学等多维度评估方法，以实现靶向铁死亡在临床中的成功应用，从而为癌症治疗开辟新的途径。原文链接：https://doi.org/10.1016/j.ccell.2024.03.011声明：发表/转载本文仅仅是出于传播信息的需要，并不意味着代表本公众号观点或证实其内容的真实性。据此内容作出的任何判断，后果自负。若有侵权，告知必删！长按关注本公众号粉丝群/投稿/授权/广告等请联系公众号助手觉得本文好看，请点这里↓

免疫疗法

2024-01-04

·Business Wire

Inspirna to Present at the 42nd Annual J.P. Morgan Healthcare Conference

NEW YORK--( BUSINESS WIRE )--Inspirna, Inc., a clinical stage biopharmaceutical company developing first-in-class cancer therapeutics, announced today that Chief Executive Officer Dr. Usman “Oz” Azam, M.D., will participate in a corporate presentation at the 42 nd Annual J.P. Morgan Healthcare Conference on Thursday, January 11, 2024 at 8:30am PT / 11:30am ET. About Inspirna Inspirna, Inc., is a privately-held clinical-stage biopharmaceutical company focused on the discovery and development of novel cancer drugs that target key pathways in cancers of high unmet need. The company is pursuing several first-in-class drug candidates. Inspirna’s lead drug candidate, ompenaclid (RGX-202), is an orally-administered small molecule that targets the CKB/SLC6A8 pathway. This pathway becomes activated in the tumors of select patients where it enables the generation of the energy molecule ATP in response to tumor hypoxia. Ompenaclid is currently being tested in multiple mid stage clinical trials in patients with advanced or metastatic RAS mutant colorectal cancer. Inspirna’s second clinical stage drug candidate, abequolixron (RGX-104), is an oral small molecule activator of LXR/APOE that inhibits angiogenesis and tumor myeloid derived suppressor cells to enhance the immune response against tumors. Abequolixron is currently being tested in a Phase 1b/2 clinical trial in patients with advanced or metastatic lung cancer in combination with docetaxel and endometrial cancer in combination with ipilimumab through a clinical collaboration with Bristol Myers Squibb. Inspirna identifies novel cancer targets using its microRNA-based target discovery platform, RNA-DRIVEr, which was originally developed by Inspirna’s scientific co-founders at The Rockefeller University and exclusively licensed to Inspirna. The Company brings together distinguished scientific founders, a seasoned board of directors, and a leadership team comprised of experienced drug developers. The Company is funded by leading biotechnology investors, including Novo Holdings A/S, Sofinnova Partners, Sands Capital, Vivo Capital, Lepu Holdings Limited, Sixty Degree Capital, Silicon Valley Bank, K2 HealthVentures, Oceanpine Capital, WuXi PharmaTech Healthcare Fund I, LP, Alexandria Venture Investments, LLC, Dreavent 6, Exor Seeds, and the Partnership Fund for New York City. For more information, please visit https://inspirna.com/ .