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Last update 23 Jan 2025

SLC1A4

Last update 23 Jan 2025

Basic Info

Synonyms

alanine/serine/cysteine/threonine transporter, Alanine/serine/cysteine/threonine transporter 1, ASCT-1

+ [6]

Introduction

Sodium-dependent neutral amino-acid transporter that mediates transport of alanine, serine, cysteine, proline, hydroxyproline and threonine.

Drugs associated with SLC1A4

WO2024121126

Patent Mining

Target

SLC1A4

Mechanism-

Active Org.

Institut régional du Cancer de Montpellier [+2]

Originator Org.

Institut National de la Santé et de la Recherche Médicale [+2]

Active Indication

Neoplasms

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with SLC1A4

100 Translational Medicine associated with SLC1A4

0 Patents (Medical) associated with SLC1A4

209

Literatures (Medical) associated with SLC1A4

01 Jan 2025·Cancer Medicine

Tandem Versus Single Autologous Stem Cell Transplantation for High‐Risk Multiple Myeloma in the Era of Novel Agents: A Real‐World Study of China

Article

Author: Dou, Xuelin ; Deng, Daoxing ; Lu, Jin ; Wen, Lei ; Wang, Fengrong ; Zhao, Peng ; Li, Jiangtao ; Liu, Hui ; Ren, Juan ; Huang, Xiaojun ; Wang, Liru ; Mo, Xiaodong ; Zhong, Yuping ; Peng, Nan ; Cao, Leqing ; Liu, Yang ; Chen, Yuan ; Bao, Li ; Liu, Xiaodan

ABSTRACTBackgroundThis study compares the efficacy and safety of single autologous stem cell transplantation (ASCT) versus tandem ASCT for multiple myeloma (MM) patients in the era of novel agents.MethodsA total of 112 high‐risk MM patients were included (single ASCT, (n = 57) or tandem ASCT(n = 55) in this retrospective multicenter study. Responses and outcomes were evaluated.ResultsAt 100 days after ASCT1 and ASCT2, 36 (63.2%) versus 45 (81.8%) patients achieved sCR/CR, 16 (28.1%) versus 7 (12.7%) patients achieved VGPR, and 5 (8.8%) versus 1 (1.8%) patient achieved PR, respectively, in the single and tandem ASCT cohorts. The 3‐year cumulative incidence of non‐relapse mortality and disease progression was 0% versus 7.3% (p = 0.083), and 45.8% versus 25.8% (p = 0.039), respectively, for the single and tandem ASCT cohort. The tandem ASCT cohort showed a trend of better 3‐year probability of PFS (58.1% vs. 64.7%, p = 0.064) compared with the single ASCT cohort. In multivariate analysis, ultra high‐risk and achieving<VGPR response after ASCT1 were associated with an inferior PFS. Ultra high‐risk was also associated with an inferior OS.ConclusionsTandem ASCT demonstrated improved outcomes compared to single ASCT in high‐risk MM patients receiving triplet or quadruplet induction and maintenance therapy. However, patients with ultra high‐risk cytogenetics may require innovative therapeutic approaches, as tendem ASCT does not overcome their adverse prognosis.

01 Dec 2024·Nature Cell Biology

NAT10-mediated mRNA N4-acetylcytidine reprograms serine metabolism to drive leukaemogenesis and stemness in acute myeloid leukaemia

Article

Author: Gao, Yijun ; Zhang, Yaojun ; Yang, Ying ; Zhang, Xiuxin ; Wang, Yushuai ; Hu, Jiacheng ; Zhang, Shilin ; Kang, Yalin ; Gao, Weiwei ; Song, Yunda ; Huang, Huilin ; Xia, Youmei ; Yang, Zhoutian ; Li, Yuanpei ; Li, Baiqing ; Long, Yifei ; Liao, Wenting ; Mo, Hongjie ; Huang, Feng ; Chen, Hongming ; Pan, Lili ; Du, Xiao ; Liang, Yang ; Weng, Hengyou ; Chen, Jianjun ; Li, Yingmin ; Wen, Yueting ; Liu, Yadi ; Wang, Yun ; Zhang, Subo ; Dong, Shenghua

RNA modification has emerged as an important epigenetic mechanism that controls abnormal metabolism and growth in acute myeloid leukaemia (AML). However, the roles of RNA N⁴-acetylcytidine (ac4C) modification in AML remain elusive. Here, we report that ac4C and its catalytic enzyme NAT10 drive leukaemogenesis and sustain self-renewal of leukaemic stem cells/leukaemia-initiating cells through reprogramming serine metabolism. Mechanistically, NAT10 facilitates exogenous serine uptake and de novo biosynthesis through ac4C-mediated translation enhancement of the serine transporter SLC1A4 and the transcription regulators HOXA9 and MENIN that activate transcription of serine synthesis pathway genes. We further characterize fludarabine as an inhibitor of NAT10 and demonstrate that pharmacological inhibition of NAT10 targets serine metabolic vulnerability, triggering substantial anti-leukaemia effects both in vitro and in vivo. Collectively, our study demonstrates the functional importance of ac4C and NAT10 in metabolism control and leukaemogenesis, providing insights into the potential of targeting NAT10 for AML therapy.

01 Dec 2024·International Journal of Biological Macromolecules

In silico analysis shows slc1a4 as a potential target of hsa-mir-133a for regulating glutamine metabolism in gastric cancer

Article

Author: Sinha, Anupriya ; Patnaik, Jayasree ; Parija, Tithi ; Chakraborty, Averi ; Patnaik, Srinivas ; Parida, Nandita

Cutting-edge research has spotlighted glutamine metabolism as a promising therapeutic target in managing gastric cancer. This investigation highlights the upregulated glutamine transporters by leveraging clinical data from the TCGA Database and the expression analysis of the transcriptome profile of stomach adenocarcinoma (STAD) patients. Notably, it identifies SLC1A4 as a potential glutamine transporter in STAD. The screening of human miRNAs conducted using the TargetScan database, and the subsequent docking analysis present multiple miRNAs with the potential of being explored as therapeutic agents. By integrating transcriptome profiling, miRNA screening, and molecular docking, this study reveals, for the first time, the potential of hsa-mir-133a-1 in targeting slc1a4, along with its known target mTOR, in stomach cancer. The myriad interactions that can be regulated by this silencing mechanism are anticipated to ultimately reduce glutamine uptake in STAD. This study provides compelling evidence of glutamine transport via SLC1A4 in stomach cancer and delves into how it might impact mTOR and some of its pivotal downstream molecules. Considering these findings, novel therapeutic strategies can be devised to further enhance existing methods for combating gastric cancer.

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SLC1A4

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