A Randomized, Double-blind, Placebo-controlled Phase 2 Study Using the Rhinovirus Challenge Model to Investigate the Efficacy and Safety of 2-Deoxy-D-Glucose as Pre-exposure Prophylaxis

2-DG-02 is a randomized, placebo-controlled, double-blind Phase 2 study to investigate the efficacy and safety of 2-Deoxy-D-Glucose as a pre-exposure prophylaxis using the rhinovirus challenge model in healthy study participants.

开始日期2024-04-02

申办/合作机构

G.ST Antivirals GmbH初创企业

CTIS2023-509311-91-01 / Recruiting

A randomized, double-blind, placebo-controlled Phase 2 study using the rhinovirus challenge model to investigate the efficacy and safety of 2-Deoxy-D-glucose as pre-exposure prophylaxis. - 2-DG-02

开始日期2024-02-14

申办/合作机构

G.ST Antivirals GmbH初创企业

NCT05314933 / Completed临床1期

A Single/Multiple Ascending Dose Phase 1 Study Of The Safety, Tolerability, And Pharmacokinetics Of Intranasal 2-Deoxy-D-Glucose In Normal Healthy Volunteers

2-DG-01 is a randomized, double-blind, placebo-controlled, single and multiple ascending dose phase 1 study assessing safety, tolerability and pharmacokinetics of 2-DG in normal healthy volunteers (NHV). The safety and pharmacokinetics of 2-DG are assessed after single or multiple intranasal administrations.

开始日期2022-03-03

申办/合作机构

G.ST Antivirals GmbH初创企业

100 项与 2-脱氧-D-葡萄糖相关的临床结果

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100 项与 2-脱氧-D-葡萄糖相关的转化医学

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100 项与 2-脱氧-D-葡萄糖相关的专利（医药）

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4,383

项与 2-脱氧-D-葡萄糖相关的文献（医药）

2024-02-01·Free radical biology & medicine

Potassium ion efflux induces exaggerated mitochondrial damage and non-pyroptotic necrosis when energy metabolism is blocked

Article

作者: Li, Ya-Ping ; Zhou, Zhi-Ya ; Zha, Qing-Bing ; Ouyang, Dong-Yun ; He, Xian-Hui ; Lu, Na ; Wong, Tak-Sui ; Gan, Ying-Qing ; Yuan, Li-Sha ; Xu, Rong

Damage-associated molecular patterns (DAMPs) such as extracellular ATP and nigericin (a bacterial toxin) not only act as potassium ion (K⁺) efflux inducers to activate NLRP3 inflammasome, leading to pyroptosis, but also induce cell death independently of NLRP3 expression. However, the roles of energy metabolism in determining NLRP3-dependent pyroptosis and -independent necrosis upon K⁺ efflux are incompletely understood. Here we established cellular models by pharmacological blockade of energy metabolism, followed by stimulation with a K⁺ efflux inducer (ATP or nigericin). Two energy metabolic inhibitors, namely CPI-613 that targets α-ketoglutarate dehydrogenase and pyruvate dehydrogenase (a rate-limiting enzyme) and 2-deoxy-d-glucose (2-DG) that targets hexokinase, are recruited in this study, and Nlrp3 gene knockout macrophages were used. Our data showed that CPI-613 and 2-DG dose-dependently inhibited NLRP3 inflammasome activation, but profoundly increased cell death in the presence of ATP or nigericin. The cell death was K⁺ efflux-induced but NLRP3-independent, which was associated with abrupt reactive oxygen species (ROS) production, reduction of mitochondrial membrane potential, and oligomerization of mitochondrial proteins, all indicating mitochondrial damage. Notably, the cell death induced by K⁺ efflux and blockade of energy metabolism was distinct from pyroptosis, apoptosis, necroptosis or ferroptosis. Furthermore, fructose 1,6-bisphosphate, a high-energy intermediate of glycolysis, significantly suppressed CPI-613+nigericin-induced mitochondrial damage and cell death. Collectively, our data show that energy deficiency diverts NLRP3 inflammasome activation-dependent pyroptosis to Nlrp3-independent necrosis upon K⁺ efflux inducers, which can be dampened by high-energy intermediate, highlighting a critical role of energy metabolism in cell survival and death under inflammatory conditions.

2024-02-01·Comparative biochemistry and physiology. Part B, Biochemistry & molecular biology

Oxidative phosphorylation rather than glycolysis is the primary energy source for sperm motility in the mussels Mytilus edulis

Article

作者: Sokolova, Inna M ; Kong, Hui

Broadcast-spawning marine mussels rely on high sperm motility for successful fertilization in the dynamic seawater environment. Mitochondria are typically considered the primary source of ATP generation via oxidative phosphorylation (OXPHOS); however, the ATP generation pathways of mussel sperm have not been fully characterized. To better understand the importance of both OXPHOS and glycolysis for mussel sperm function, we conducted experiments inhibiting these pathways in sperm from Mytilus edulis. Our results indicate that oligomycin, an inhibitor of the mitochondrial ATP synthase, immediately decreased sperm motility rate, velocity, and ATP content, while 2-deoxy-d-glucose, a glycolysis inhibitor, had no effect. The OXPHOS inhibitor rotenone also partially reduced sperm motility rate and velocity. Interestingly, no evidence was found for the inhibitors' effects on the content of energy-rich compounds (lipids, carbohydrates, and proteins) in the mussels' sperm, indicating only modest energy demand to fuel sperm motility. Based on these findings, we conclude that OXPHOS is the primary energy source for sperm motility in marine mussels. Our study sheds light on the intricacies of mussel sperm physiology and highlights the importance of understanding the energy requirements for successful fertilization in broadcast-spawning marine invertebrates.

2024-02-01·Neurochemical research

Modulation of Cellular Levels of Adenosine Phosphates and Creatine Phosphate in Cultured Primary Astrocytes

Article

作者: Berger, Julius ; Karger, Gabriele ; Dringen, Ralf

Abstract:

Adenosine triphosphate (ATP) is the main energy currency of all cells, while creatine phosphate (CrP) is considered as a buffer of high energy-bond phosphate that facilitates rapid regeneration of ATP from adenosine diphosphate (ADP). Astrocyte-rich primary cultures contain ATP, ADP and adenosine monophosphate (AMP) in average specific contents of 36.0 ± 6.4 nmol/mg, 2.9 ± 2.1 nmol/mg and 1.7 ± 2.1 nmol/mg, respectively, which establish an adenylate energy charge of 0.92 ± 0.04. The average specific cellular CrP level was found to be 25.9 ± 10.8 nmol/mg and the CrP/ATP ratio was 0.74 ± 0.28. The specific cellular CrP content, but not the ATP content, declined with the age of the culture. Absence of fetal calf serum for 24 h caused a partial loss in the cellular contents of both CrP and ATP, while application of creatine for 24 h doubled the cellular CrP content and the CrP/ATP ratio, but did not affect ATP levels. In glucose-deprived astrocytes, the high cellular ATP and CrP contents were rapidly depleted within minutes after application of the glycolysis inhibitor 2-deoxyglucose and the respiratory chain inhibitor antimycin A. For those conditions, the decline in CrP levels always preceded that of ATP contents. In contrast, incubation of glucose-fed astrocytes for up to 30 min with antimycin A had little effect on the high cellular ATP content, while the CrP level was significantly lowered. These data demonstrate the importance of cellular CrP for maintaining a high cellular ATP content in astrocytes during episodes of impaired ATP regeneration.

项与 2-脱氧-D-葡萄糖相关的新闻（医药）

2024-05-20

·PRNewswire

Studies Show Linked Biological Pathways Driving Skin Inflammation

NEW YORK, May 20, 2024 /PRNewswire/ -- A certain biological pathway, a set of linked reactions in the body, drives the inflammation seen in the skin disease psoriasis, a new study finds. The work could lead to improved therapies for all inflammatory skin diseases, including atopic and allergic dermatitis and a type of boil called hidradenitis suppurativa, say the study authors. Inflammation is the body's natural response to irritation and infection, but when out of control, it can lead to the reddish, flaky, itchy lesions that come with these skin diseases. Led by researchers at NYU Langone Health, the new study found that the interleukin-17 (IL-17) pathway, whose activity is blocked by existing anti-inflammatory drugs, activates a protein called hypoxia inducible factor 1-alpha (HIF-1-alpha) in psoriasis. Researchers say that IL-17 has long been known to be active in inflammation, but the role of HIF-1-alpha has until now been unclear. The research team also found that HIF-1-alpha let inflamed skin cells more actively break down sugar for energy, supporting their metabolism and leading to the production of a waste product called lactate. When consumed by inflammatory T cells, lactate triggered production of IL-17, fueling even more inflammation. Publishing in the journal Immunity online May 20, the findings show that in human skin tissue samples from people with psoriasis, measures of gene activity around IL-17 and HIF-1-alpha were similar, suggesting that these factors are interconnected. Experiments in mice treated to develop psoriasis found that subsequent treatment with an experimental drug that blocks the action of HIF-1-alpha, called BAY-87-2243, resolved inflammatory skin lesions. Further, skin samples from 10 patients successfully treated with anti-inflammatory drug etanercept showed diminished activity for both IL-17 and HIF-1-alpha, suggesting to researchers that when IL-17 is blocked, so is HIF-1-alpha. "Our study results broadly show that activation of HIF-1-alpha is at the crux of metabolic dysfunction observed in psoriasis and that its action is triggered by IL-17, another key inflammatory-signaling molecule," said corresponding study author Shruti Naik, PhD, associate professor at NYU Grossman School of Medicine in the Departments of Pathology and Medicine, and the Ronald O. Perelman Department of Dermatology. Further experiments were performed on skin samples from five patients with psoriasis whose healthy and inflamed skin was separately treated with either BAY-87-2243 or an existing combination of topical drugs (calcipotriene and betamethasone dipropionate). Researchers then compared differences in inflammatory gene activity as a measure of impact and found that the HIF-1-alpha inhibitor had a greater effect than existing topical drugs. Specifically, skin samples that responded to HIF-1-alpha therapy had 2,698 genes that were expressed differently, while standard-of-care–treated samples had 147 differently expressed genes. Genetic analysis of skin samples from another 24 psoriatic patients treated with the IL-17A–blocking drug secukinumab showed only decreased, not heightened, gene activity connected to HIF-1-alpha when compared to HIF-1-alpha gene activity in nine healthy patients with no psoriatic disease. Researchers say this indicates HIF-1-alpha's blocked action was codependent on blockage of IL-17. Additional experiments in mice showed that blocking sugar (glucose) uptake in the skin slowed psoriatic disease growth by limiting glucose metabolism, or glycolysis. Both the number of immune T cells tied to inflammation and the cell levels of IL-17 also decreased. The researchers found further that levels of lactate, the main byproduct of glycolysis, in psoriatic skin cell cultures dropped once exposed to the glycolysis-inhibiting drug 2-DG. Directly targeting lactate production in psoriatic mice using a topical skin cream containing lactate dehydrogenase, which breaks down lactate, also slowed disease progression in the skin, with reduced numbers of inflammatory gamma-delta T cells and reduced IL-17 activity. Gamma-delta T cells were shown to take up lactate and use it to produce IL-17. "Our findings suggest that blocking either HIF-1-alpha's action or its glycolytic metabolic support mechanisms could be effective therapies for curbing the inflammation," added Naik, who is also the associate director for NYU Langone's Judith and Stewart Colton Center for Autoimmunity. "Evidence of HIF-1-alpha's depressed action, or downregulation, could also serve as a biomarker, or molecular sign, that other anti-inflammatory therapies are working," said study co-senior investigator Jose U. Scher, MD, the Steere Abramson Associate Professor of Medicine in the Department of Medicine at NYU Grossman School of Medicine. Scher, who also serves as director of NYU Langone's Psoriatic Arthritis Center and the Judith and Stewart Colton Center for Autoimmunity, says the team plans to develop experimental drugs that can block HIF-1-alpha and lactate action in the skin "to end the underlying vicious cycle of IL-17–driven inflammation in skin disease. Our research fundamentally expands the scope of feasible therapeutic options." Naik points out that while many available therapies for psoriasis, including steroids and immunosuppressive drugs, reduce inflammation and symptoms, they do not cure the disease. She said further experiments are needed to refine which experimental drug works best, with respect to HIA-1-alpha inhibition, before clinical trials could start. Indeed, Naik and study co-lead investigators Ipsita Subudhi and Piotr Konieczny have a patent application pending (U.S. application number 63/540,794) for inflammatory skin disease therapies derived from their work on HIA-1-alpha inhibition. More than 8 million Americans and 125 million worldwide are estimated to have psoriatic disease. The condition affects men and women equally. Funding support for the studies was provided by National Institutes of Health grants P30AR075043, R01AR080436, R01AI168462, UC2AR081029, K22AI135099, K99AR083536, T32AR069515, TL1TR001447, UL1TR001445, and DP2AR079173. Additional funding was provided by the National Psoriasis Foundation, the Judith and Stewart Colton Center for Autoimmunity, the Beatrice Snyder Foundation, the Riley Family Foundation, the American Association of Immunologists, the International Human Frontier Science Program, the Charles H. Revson Foundation, and the Pew-Stewart Scholar Award 00034119, as well as the New York Stem Cell Foundation. Naik serves on the advisory boards of Seed Inc. and as a consultant for BiomX. She also receives research funding from Takeda Pharmaceuticals. Scher has served as a consultant for Janssen, Pfizer, UCB, and BMS. He also receives research funding from Janssen and Pfizer. All of these arrangements are being managed in accordance with the policies and practices of NYU Langone Health. Besides Naik, Scher, Subudhi, and Konieczny, other NYU Langone investigators were Aleksandr Prystupa, Rochelle Castillo, Erica Sze-Tu, Yue Xing, Daniel Rosenblum, Ilana Reznikov, Ikjot Sidhu, Cynthia Loomis, Catherine Lu, and Aristotelis Tsirigos. Other study co-investigators were Niroshana Anandasabapathy, at Weill Cornell Medicine; Mayte Suarez-Farinas, at the Icahn School of Medicine at Mount Sinai; and Johann Gudjonsson, at the University of Michigan. Contact: Gregory Williams, [email protected] SOURCE NYU Langone Health

临床结果

2024-05-13

·BioSpace

HUTCHMED Initiates the RAPHAEL Registrational Phase III Trial of HMPL-306 for Patients with IDH1- and/or IDH2-Mutated Relapsed/Refractory Acute Myeloid Leukemia in China

HONG KONG and SHANGHAI, China and FLORHAM PARK, N.J., May 14, 2024 (GLOBE NEWSWIRE) -- HUTCHMED (China) Limited (“HUTCHMED”) (Nasdaq/AIM:HCM; HKEX:13) today announces that it has initiated a registrational Phase III clinical trial of HMPL-306 in patients with mutated isocitrate dehydrogenase (“IDH”) 1 or 2 relapsed / refractory acute myeloid leukemia (“AML”) in China. The first patient received their first dose on May 11, 2024. HMPL-306 is a novel dual-inhibitor of IDH1 and IDH2 enzymes. Mutations of IDH1 and IDH2 have been implicated as drivers of certain hematological malignancies, gliomas and solid tumors, particularly among AML patients. Although some IDH inhibitors have been approved in certain markets for AML, isoform switching between the cytoplasmic mutant IDH1 and mitochondrial mutant IDH2 often leads to acquired resistance to single inhibitors of IDH1 or IDH2. Targeting both IDH1 and IDH2 mutations may provide therapeutic benefits in cancer patients by overcoming this acquired resistance. RAPHAEL is a multicenter, randomized, open-label, registrational Phase III clinical trial designed to evaluate the safety and efficacy of HMPL-306 as a monotherapy in patients with relapsed or refractory AML harboring IDH1 and/or IDH2 mutations. The primary endpoint of overall survival (OS) and the secondary endpoints, including event-free survival (EFS) and complete remission (“CR”) rate, will be tested in comparison with current salvage chemotherapy regimens. The Company is looking to enroll approximately 320 patients for this registrational study, which is being led by principal investigator Prof Xiaojun Huang of Peking University People’s Hospital. Additional details may be found at clinicaltrials.gov, using identifier NCT06387069. The study follows positive data from a two-stage, open-label Phase I study evaluating the safety, pharmacokinetics, pharmacodynamics and efficacy of HMPL-306 in this indication (NCT04272957). The first-in-human dose-escalation stage data was presented at the European Hematology Association Congress (“EHA”) in June 2023.1 Results of the dose expansion stage of the study in over 50 patients demonstrated promising CR rates at the recommended Phase II dose are expected to be presented at the EHA Congress in June 2024. About IDH and Hematological Malignancies IDHs are critical metabolic enzymes that help to break down nutrients and generate energy for cells. When mutated, IDH creates a molecule that alters the cell’s genetic programming and prevents cells from maturing. IDH1 or IDH2 mutations are common genetic alterations in various types of blood and solid tumors, including AML with approximately 14-20% of patients having mutant IDH genes, myelodysplastic syndrome (MDS), myeloproliferative neoplasms (MPNs), low-grade glioma and intrahepatic cholangiocarcinoma. Mutant IDH isoform switching, either from cytoplasmic mutant IDH1 to mitochondrial mutant IDH2, or vice versa, is a mechanism of acquired resistance to IDH inhibition in AML and cholangiocarcinoma.2,3,4 According to the National Cancer Institute (NCI), there will be approximately 20,380 new cases of AML in the U.S. in 2023 and the five-year relative survival rate is 31.7%5. Currently, the U.S. Food and Drug Administration (FDA) has approved two drugs for IDH1 mutation and one drug for IDH2 mutation, but no dual inhibitor targeting both IDH1 and IDH2 mutants has been approved. There were an estimated 19,700 new cases of AML in China in 2018 and is estimated to reach 24,200 in China in 2030.6 In China one IDH1 inhibitor was approved in 2022. About HUTCHMED HUTCHMED (Nasdaq/AIM:HCM; HKEX:13) is an innovative, commercial-stage, biopharmaceutical company. It is committed to the discovery, global development and commercialization of targeted therapies and immunotherapies for the treatment of cancer and immunological diseases. It has approximately 5,000 personnel across all its companies, at the center of which is a team of about 1,800 in oncology/immunology. Since inception, HUTCHMED has focused on bringing cancer drug candidates from in-house discovery to patients around the world, with its first three medicines now marketed in China, the first of which is also marketed in the U.S. For more information, please visit: or follow us on LinkedIn. Forward-Looking Statements This press release contains forward-looking statements within the meaning of the “safe harbor” provisions of the U.S. Private Securities Litigation Reform Act of 1995. These forward-looking statements reflect HUTCHMED’s current expectations regarding future events, including its expectations regarding the therapeutic potential of HMPL-306 for the treatment of patients with relapsed or refractory AML and the further development of HMPL-306 in this and other indications. Forward-looking statements involve risks and uncertainties. Such risks and uncertainties include, among other things, assumptions regarding the timing and outcome of clinical studies and the sufficiency of clinical data to support an NDA submission of HMPL-306 for the treatment of patients with relapsed or refractory AML or other indications in China or other jurisdictions, its potential to gain approvals from regulatory authorities on an expedited basis or at all, the efficacy and safety pro HMPL-306, HUTCHMED’s ability to fund, implement and complete its further clinical development and commercialization plans for HMPL-306 and the timing of these events. Existing and prospective investors are cautioned not to place undue reliance on these forward-looking statements, which speak only as of the date hereof. For further discussion of these and other risks, see HUTCHMED’s filings with the U.S. Securities and Exchange Commission, The Stock Exchange of Hong Kong Limited and on AIM. HUTCHMED undertakes no obligation to update or revise the information contained in this press release, whether as a result of new information, future events or circumstances or otherwise. Medical Information This press release contains information about products that may not be available in all countries, or may be available under different trademarks, for different indications, in different dosages, or in different strengths. Nothing contained herein should be considered a solicitation, promotion or advertisement for any prescription drugs including the ones under development. CONTACTS Investor Enquiries +852 2121 8200 / ir@hutch-med.com Media Enquiries Ben Atwell / Alex Shaw, FTI Consulting +44 20 3727 1030 / +44 7771 913 902 (Mobile) / +44 7779 545 055 (Mobile) / HUTCHMED@fticonsulting.com Zhou Yi, Brunswick +852 9783 6894 (Mobile) / HUTCHMED@brunswickgroup.com Nominated Advisor Atholl Tweedie / Freddy Crossley / Daphne Zhang, Panmure Gordon +44 (20) 7886 2500 _______________________ REFERENCES 1 Hu L et al. P539: A Phase 1 Study of HMPL-306, a Dual Inhibitor of Mutant Isocitrate Dehydrogenase (IDH) 1 and 2, in Patients with Relapsed/Refractory Myeloid Hematological Malignancies Harboring IDH1 and/or 2 Mutations. Hemasphere. 2023;7(Suppl):e86312d3. Published 2023 Aug 8. doi:10.1097/01.HS9.0000969064.86312.d3. 2 S Choe S et al. Blood 2019;134(Supplement_1):545. doi:10.1182/blood-2019-122671. 3 Harding JJ et al. Isoform Switching as a Mechanism of Acquired Resistance to Mutant Isocitrate Dehydrogenase Inhibition. Cancer Discov. 2018;8(12):1540-1547. doi:10.1158/2159-8290.CD-18-0877. 4 Delahousse J et al. Circulating oncometabolite D-2-hydroxyglutarate enantiomer is a surrogate marker of isocitrate dehydrogenase-mutated intrahepatic cholangiocarcinomas. Eur J Cancer. 2018;90:83-91. doi:10.1016/j.ejca.2017.11.024. 5 Source: National Cancer Institute – seer.cancer.gov/statfacts/html/amyl.html. 6 Lin J et al. IDH1 and IDH2 mutation analysis in Chinese patients with acute myeloid leukemia and myelodysplastic syndrome. Ann Hematol. 2012;91(4):519-525. doi:10.1007/s00277-011-1352-7.

临床1期临床2期临床结果临床3期免疫疗法

2024-04-01

·今日头条

双抑制剂组合！显著增强抗肿瘤效果！复旦大学郭伟剑团队发现胃癌治疗潜在靶点

本文为转化医学网原创，转载请注明出处作者：Jerry 导读：转移是癌症治疗的瓶颈，研究表明长链非编码RNAs(lncRNAs)在调节癌症转移中发挥着关键作用，但对lncRNAs在胃癌中的研究仍有限。 3月29日，复旦大学郭伟剑研究团队在期刊《Cell Death&Disease》上发表了题为“LncRNA SNHG26 promotes gastric cancer progression and metastasis by inducing c-Myc protein translation and an energy metabolism positive feedback loop”的研究论文。本研究中，功能实验表明，SNHG26在体内外均可促进细胞上皮-间充质转化和增殖。机制上，SNHG26与核仁素(NCL)相互作用，通过增加c-Myc的转化来调节其表达，进而通过己糖激酶2(HK2)促进能量代谢，从而促进胃癌恶性发展。能量代谢的增加为促进c-Myc的转化和表达提供了足够的能量，形成了正反馈循环。此外，代谢和转化抑制剂可以阻断这一循环，从而抑制细胞增殖和迁移，且两种抑制剂联合应用可增强抗肿瘤效果，提示其在GC 治疗中具有潜在的治疗前景。 https://www-nature-com.libproxy1.nus.edu.sg/articles/s41419-024-06607-8#Sec36 研究背景 01 胃癌（GC）是人类第五种常见的肿瘤，每年估计有超过100万新病例。由于其高转移频率，GC 是导致癌症相关死亡的第四大原因，超过60% 的患者在诊断时呈现局部或远处转移。尽管在分子靶向药物和免疫治疗方面取得了实质性进展，但由于转移的存在，GC 患者的5年生存率仍然不理想。因此，迫切需要对 GC 转移机制进行调查，以开发新的治疗方法。长链非编码RNA(lncRNA)超过200个核苷酸，具有有限的蛋白质编码能力。lncRNA被广泛表达，并在基因调控中发挥关键作用。lncRNA通过与RNA、DNA和蛋白质相互作用发挥多种功能。大量研究表明，lncRNA的异常表达与癌细胞行为相关。lncRNA BDNF-AS/WDR5/FBXW7轴通过调节VDAC3泛素化介导胃癌腹膜转移中的铁死亡。lncRNA TNFRSF10A-AS1通过与MPZL1结合促进胃癌进展。然而，由于lncRNA数量众多，其机制复杂，我们对胃癌中lncRNA的认识仍然有限。研究进展 02 为了证实SNHG26在体内的致癌作用，研究人员首先通过将过表达SNHG26的MKN-28细胞注射到裸鼠皮下生成皮下肿瘤模型。4周后，将小鼠处死，并称量肿瘤。SNHG26过表达组的肿瘤比对照组大，表明SNHG26可以促进肿瘤生长。接下来，研究人员将过表达SNHG26的MKN-28细胞注射到裸鼠尾静脉中，以评估转移能力。8周后，将小鼠处死，并量化肺中的转移位点。此外，HE染色显示SNHG26过表达组的肺部转移位点数量显著高于对照组。而且，皮下肿瘤的免疫组化显示SNHG26过表达后E-cad表达降低。总的来说，体内外结果表明SNHG26促进胃癌的增殖和转移。研究还表明，SNHG26通过c-Myc/HK2途径介导糖酵解和能量代谢，促进胃癌细胞的增殖和迁移，糖酵解代谢增加提供能量促进mRNA转化，形成正反馈循环，代谢和转化抑制剂阻断该正反馈循环作用，抑制癌细胞增殖和迁移。两者联合抑制可增加抗肿瘤效果，提示其在胃癌治疗中具有潜在的治疗前景。转化抑制剂(CX-5461)和代谢抑制剂(2-DG)的联合使用在体内和体外均有显著的治疗效果研究结论 03 总之，研究人员发现了一种新的lncRNA SNHG26，它在胃癌中表达上调。 SNHG26与NCL相互作用，通过增加c-Myc的转化促进胃癌的增殖和转移。本研究揭示了lncRNA在转化和转移之间的新机制，表明SNHG26/NCL/c-Myc轴是胃癌的潜在治疗靶点。参考资料： https://www-nature-com.libproxy1.nus.edu.sg/articles/s41419-024-06607-8#Sec36 注：本文旨在介绍医学研究进展，不能作为治疗方案参考。如需获得健康指导，请至正规医院就诊。热门·直播/活动 🕓 上海｜06月14日-16日 ▶ 第六届上海国际癌症大会将于6月14-16日在上海举办，学科交叉，共同推进肿瘤研究与诊治多模态！ 🕓 北京｜09月20日-21日 ▶ 第五届单细胞技术应用研讨会暨空间组学前沿研讨会欢迎您的参与！点击对应文字查看详情

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100 项与 2-脱氧-D-葡萄糖相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
-	-	-	DB08831

研发状态

批准上市

10 条最早获批的记录,

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适应症	国家/地区	公司	日期
新型冠状病毒感染	印度	Dr. Reddy's Laboratories Ltd.	2021-05-01

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适应症	最高研发状态	国家/地区	公司	日期
普通感冒	临床2期	荷兰	G.ST Antivirals GmbH初创企业	2024-04-02
鼻病毒感染	临床2期	荷兰	G.ST Antivirals GmbH初创企业	2024-04-02
前列腺癌	临床2期	美国	Defense Language Institute Foreign Language Center	2006-11-01
晚期恶性实体瘤	临床1期	美国	Threshold Pharmaceuticals, Inc.	2004-02-01
乳腺癌	临床1期	美国	Threshold Pharmaceuticals, Inc.	2004-02-01
头颈部肿瘤	临床1期	美国	Threshold Pharmaceuticals, Inc.	2004-02-01
肺癌	临床1期	美国	Threshold Pharmaceuticals, Inc.	2004-02-01
胰腺癌	临床1期	美国	Threshold Pharmaceuticals, Inc.	2004-02-01
胃癌	临床1期	美国	Threshold Pharmaceuticals, Inc.	2004-02-01

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研究	分期	人群特征	评价人数	分组	结果	评价	发布日期


ERS2019	N/A	间皮瘤	-	Cisplatin+Pemetrexed	艱艱願夢淵齋顧選餘醖(築膚簾鑰艱觸繭觸醖網) = 繭膚膚壓糧觸壓憲鏇憲簾顧衊願襯鏇積艱網觸 (構衊鏇願艱壓觸鏇築夢 )	-	2019-09-28
ERS2019	N/A	间皮瘤	-	2-Deoxy-glucose (2DG)+Cisplatin+Pemetrexed	艱艱願夢淵齋顧選餘醖(築膚簾鑰艱觸繭觸醖網) = 鏇積艱鬱糧繭憲壓繭夢簾顧衊願襯鏇積艱網觸 (構衊鏇願艱壓觸鏇築夢 )	-	2019-09-28
MP88-06 (AUA2016)	N/A	膀胱癌	-	2-deoxyglucose (2DG)	窪鏇顧膚積製範糧餘積(襯壓觸淵衊繭夢積鑰夢) = 窪蓋艱淵憲顧範鹹簾構艱艱膚夢鏇夢選簾膚餘 (夢鑰積鑰齋遞蓋構壓繭 ) 更多	-	2016-04-01
ASN2014	N/A	多囊肾	-	2-deoxyglucose (2DG)	獵鏇遞鹽觸築積選膚鏇(鹽膚襯簾製醖簾窪襯鏇) = 網蓋糧艱積製襯糧鏇簾願獵壓鹹淵齋鹹鬱遞鹽 (糧鏇獵壓網鑰構遞觸選 ) 更多	-	2014-11-11
ASN2014	N/A	多囊肾	-	Vehicle treatment	獵鏇遞鹽觸築積選膚鏇(鹽膚襯簾製醖簾窪襯鏇) = 觸衊網齋艱壓願窪顧鏇願獵壓鹹淵齋鹹鬱遞鹽 (糧鏇獵壓網鑰構遞觸選 ) 更多	-	2014-11-11
SP018 (ERA2014)	N/A	多囊肾	-	2-deoxyglucose (2-DG)	願鏇衊鬱築獵選蓋齋繭(襯襯糧鹹鬱願膚簾衊壓) = inhibited 艱鑰選築鹽壓艱淵鏇淵 (遞衊衊鬱憲觸積齋壓夢 ) 更多	积极	2014-05-01
NCT00633087 (CTgov)	临床1/2期	晚期癌症 \| 去势抵抗性前列腺癌	12	2-deoxyglucose	壓壓築鹹鏇憲觸構蓋範(廠淵蓋製構製築窪顧獵) = 艱鬱鹽齋鏇夢觸鏇餘艱製廠願遞觸鹹鏇鏇獵糧 (餘願糧蓋簾觸膚窪糧醖, 襯蓋艱範醖壓鏇淵糧壓 ~ 壓壓齋簾鑰襯齋鑰築範) 更多	-	2014-01-07
NCT00096707 (Pubmed \| Cancer Chemother Pharmacol)	临床1期	HR阳性/HER2低表达实体瘤	-	2-deoxy-D-glucose	廠鏇選範鑰鹹製獵壓衊(蓋糧窪廠選鹹獵廠憲顧) = 齋壓獵築壓艱醖窪餘網鏇糧製鏇憲顧蓋醖獵鏇 (淵艱襯獵壓窪網衊壓壓 ) 更多	-	2013-02-01
AACR2010	临床1/2期	HR阳性/HER2低表达实体瘤 \| 去势抵抗性前列腺癌	12	2-Deoxyglucose	淵鬱網鏇膚遞繭範廠鏇(簾襯艱憲蓋構觸製糧簾) = 窪積鹹網鬱遞鹽獵獵鑰觸顧鏇衊鏇艱膚衊獵膚 (繭膚繭憲衊簾夢廠廠鹽 ) 更多	-	2010-04-15
ARVO2003	N/A	腱鞘囊肿	-	2-deoxy-D-glucose (2DG)	壓獵願艱網蓋鬱觸鏇鹽(網憲鑰築獵衊淵構觸願) = 艱獵積膚鹹糧壓襯窪窪構鬱簾壓憲膚獵鏇製餘 (製鹽獵衊鏇獵構餘鹹淵 )	-	2003-05-01
ARVO2003	N/A	腱鞘囊肿	-	Saline	壓獵願艱網蓋鬱觸鏇鹽(網憲鑰築獵衊淵構觸願) = 窪構廠獵顧窪膚範襯願構鬱簾壓憲膚獵鏇製餘 (製鹽獵衊鏇獵構餘鹹淵 )	-	2003-05-01