Last update 01 Nov 2024

BBOX

Last update 01 Nov 2024

Basic Info

Synonyms

BBH, BBOX, BBOX1

+ [6]

Introduction

Catalyzes the formation of L-carnitine from gamma-butyrobetaine.

Drugs associated with BBOX

Meldonium hydrate

Target

BBOX x SLC22A5

Mechanism

BBOX antagonists [+1]

Active Org.

Nanjing HUAXIN Biopharm. Co., Ltd. [+2]

Originator Org.-

Active Indication

Alcoholism [+4]

Inactive Indication

Cerebrovascular Disorders

Drug Highest PhaseApproved

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with BBOX

CTIS2023-509804-14-00 / Not yet recruitingIIT

The role of meldonium and individualized physical activities in the treatment of patients with heart failure - MELD-PHYS-2023

Start Date27 Mar 2024

Sponsor / Collaborator-

NCT06648902 / CompletedPhase 1/2IIT

A Phase 1/2 Study of the Safety and Preliminary Efficacy of Meldonium in Patients with Metastatic Renal Cell Carcinoma and Treatment-associated Fatigue.

Fatigue is a prevalent adverse event associated with systemic therapy using tyrosine kinase inhibitors (TKIs). Meldonium, a fatty acid oxidation inhibitor, modifies the carnitine pathway, a nutrient critical for fat metabolism. The World Anti-Doping Agency (WADA) classified meldonium as a banned substance due to its documented use by athletes aiming to enhance physical performance. In this study, the safety and preliminary efficacy of meldonium in treatment-related fatigue will be assessed.

Start Date01 Feb 2022

Sponsor / Collaborator-

CTR20140220 / SuspendedPhase 3

评估标准加米屈肼治疗慢性缺血性心力衰竭患者有效性和安全性的双盲、随机、安慰剂平行对照、多中心临床研究

[Translation] A double-blind, randomized, placebo-controlled, multicenter clinical study to evaluate the efficacy and safety of standard plus meldonium in the treatment of patients with chronic ischemic heart failure

主要目标：评估标准治疗加米屈肼相比较于标准治疗加安慰剂治疗慢性缺血性心衰病人 (NYHA II- III 级）的疗效次要目标：评估米屈肼治疗慢性缺血性心衰病人的安全性

[Translation]

Primary objective: To evaluate the efficacy of meldonium plus standard therapy compared with standard therapy plus placebo in patients with chronic ischemic heart failure (NYHA class II-III) Secondary objective: To evaluate the safety of meldonium in patients with chronic ischemic heart failure

Start Date14 Jul 2014

Sponsor / Collaborator

Jsc Grindeks

[+1]

100 Clinical Results associated with BBOX

100 Translational Medicine associated with BBOX

0 Patents (Medical) associated with BBOX

195

Literatures (Medical) associated with BBOX

01 Dec 2024·Biochimica et Biophysica Acta (BBA) - Molecular Cell Research

BBOX1 mediates metabolic reprogramming driven by hypoxia and participates in the malignant progress of high-grade serous ovarian cancer

Article

Author: Kang, Fuli ; Wei, Heng ; Wang, Ning ; Huang, Jiazhen ; Tan, Shuang ; Tang, Ying ; Wei, Wei ; Lin, Lin ; Li, Yibing ; Lu, Xiaohang

High-grade serous ovarian cancer (HGSOC) is the most aggressive type of ovarian cancer that causes great threats to women's health. Therefore, we performed RNA-sequencing technology in clinical samples to explore the molecular mechanisms underlying the progression of HGSOC. We then noticed BBOX1, a kind of 2-oxoglutarate-dependent enzyme that is highly expressed in HGSOC tumor tissues. Functional studies showed that BBOX1 promotes cell survival and growth of HGSOC cells in vitro and in vivo. Overexpression of the wild-type BBOX1 promoted cell proliferation, but the Asn191 and Asn292 mutation (key amino acid for the enzymatic activity of BBOX1) counteracted this effect (P < 0.05), which indicated that the promotion effect of BBOX1 on HGSOC cell proliferation was related to its catalytic activity. Downregulation of BBOX1 reduced the activity of the mTORC1 pathway, and decreased protein expression of IP3R3 and phosphorylation level of S6K^Thr389. Metabolomics analysis revealed that BBOX1 is implicated in the glucose metabolism, amino acid metabolism, and nucleotide metabolism of HGSOC cells. In addition, inhibition of BBOX1 suppressed HGSOC cell glycolysis and decreased glucose consumption, lactate production, and the expression of key factors in glycolysis. Finally, we found hypoxia induced the expression of BBOX1 in HGSOC cells and confirmed that BBOX1 could be transcriptionally activated by hypoxia-inducible factor-1α, which could directly bind to the BBOX1 promoter. In summary, BBOX1 mediated the metabolic reprogramming driven by hypoxia, and affected cell metabolism through the mTORC1 pathway, thus acting as an oncogene during HGSOC development.

01 Sep 2024·Poultry Science

Whole genome resequencing reveals the adaptability of native chickens to drought, tropical and frigid environments in Xinjiang

Article

Author: Zhang, Lihua ; Wu, Yingping ; Zhao, Xiaoyu ; Yao, Yingying ; Li, Haiying ; Wang, Lin ; Yao, Yang ; Li, Jiahui

Chickens exhibit extensive genetic diversity and are distributed worldwide. Different chicken breeds have evolved to thrive in diverse environmental conditions. However, research on the genetic mechanisms underlying chicken adaptation to extreme environments, such as tropical, frigid and drought-prone regions, remains limited. In this study, we conducted whole-genome sequencing of 240 individuals from six native chicken breeds in Xinjiang, China, as well as 4 publicly available chicken breeds inhabiting regions with varying annual precipitations, temperatures, and altitudes. Our analysis revealed several genetic variants among the examined breeds. Furthermore, we investigated the genetic diversity and population structure of breeds residing in extreme drought and temperature environments by comparing them. Notably, native chicken breeds exhibited different genetic diversity and population structures. Moreover, we identified candidate genes associated with chicken adaptability to the environment, such as CORO2A, CTNNA3, AGMO, GRID2, BBOX1, COL3A1, INSR, SOX5, MAP2 and PLPPR1. Additionally, pathways such as lysosome, cysteine and methionine metabolism, glycosaminoglycan degradation, and Wnt signaling may be play crucial roles in regulating chicken adaptation to drought environments. Overall, these findings contribute to our understanding of the genetic mechanisms governing chicken adaptation to extreme environments, and also offer insights for enhancing the resilience of chicken breeds to different climatic conditions.

01 Aug 2024·Molecular and Cellular Biochemistry

Regulation of tumorigenesis and ferroptosis in non-small cell lung cancer by a novel BBOX1-AS1/miR-326/PROM2 axis.

Article

Author: Shi, Jiang ; Lv, Yuanjun ; Luo, Junfang ; Ren, Jie ; Yang, Chao ; Zhang, Yang ; Li, Yuning ; An, Jinlu

Dysregulation of long non-coding RNAs (lncRNAs) is associated with the tumorigenesis and ferroptosis of non-small cell lung cancer (NSCLC). BBOX1 antisense RNA 1 (BBOX1-AS1) functions as an oncogenic driver in NSCLC. Here, we aim to investigate the regulation effect and underlying mechanism of BBOX1-AS1 in NSCLC progression and ferroptosis. RNA expression was detected by quantitative real-time PCR (qRT-PCR), and protein expression was measured by immunoblotting. Cell growth was assessed by CCK-8 and colony formation assays. Transwell assay was applied to evaluate cell invasion and migration. RNA pull-down and dual-luciferase reporter assays were applied to verify the relationship between miR-326 and BBOX1-AS1 or prominin 2 (PROM2). The role of BBOX1-AS1 in NSCLC tumorigenicity was also analyzed by xenograft assays. Silencing BBOX1-AS1 or PROM2 impeded NSCLC cell growth, migration, and invasion. Silencing BBOX1-AS1 induced cell apoptosis and ferroptosis. BBOX1-AS1 up-regulated PROM2 expression, and re-expression of PROM2 reversed the effects of BBOX1-AS1 depletion on cell malignant phenotypes and ferroptosis. BBOX1-AS1 post-transcriptionally modulated PROM2 expression by sponging miR-326. MiR-326 was validated as a mediator of BBOX1-AS1 in regulating NSCLC cell malignant phenotypes and ferroptosis. Additionally, BBOX1-AS1 deficiency in vivo resulted in the suppression of xenograft tumor growth. Together, our study defines a novel BBOX1-AS1/miR-326/PROM2 axis in regulating NSCLC malignant progression and ferroptosis, offering new evidence for the oncogenic role of BBOX1-AS1 in NSCLC. These findings may provide a basis for the future usage of targeting BBOX1-AS1 in NSCLC treatment.

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