Trolox

Vitamin E analog

Trolox

Vitamin E analog

From: 75 USD
Catalog #
(Select a product)
Vitamin E analog
Add to Wish List

Overview

Trolox is a cell-permeable and hydrophilic analog of vitamin E (Choe et al.; Lee et al.). In mice, Trolox has been shown to suppress osteoclast formation by downregulating receptor activator of NF-κB ligand (RANKL) induction and c-Fos expression (Lee et al.). Trolox also prevents cisplatin-induced apoptosis in renal epithelial cells (Xiao et al.).

DIFFERENTIATION
· Induces beta-like cell differentiation from human embryonic stem cells (Petersen et al.).
CANCER RESEARCH
· Enhances arsenic-mediated apoptosis in myeloma and breast cancer cells (Diaz et al.).
Alternative Names
6-Hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid
Cell Type
Cancer Cells and Cell Lines, Pancreatic Cells
Application
Differentiation
Area of Interest
Cancer, Stem Cell Biology
CAS Number
53188-07-1
Chemical Formula
C14H18O4
Molecular Weight
250.3 g/mol
Purity
≥ 98%
Pathway
WNT

Protocols and Documentation

Find supporting information and directions for use in the Product Information Sheet or explore additional protocols below.

Document Type
Product Name
Catalog #
Lot #
Language
Product Name
Trolox
Catalog #
100-0572, 100-0573
Lot #
All
Language
English
Document Type
Safety Data Sheet
Product Name
Trolox
Catalog #
100-0572, 100-0573
Lot #
All
Language
English

Resources and Publications

Publications (5)

Trolox-induced cardiac differentiation is mediated by the inhibition of Wnt/$\beta$-catenin signaling in human embryonic stem cells. M. S. Choe et al. Cell biology international 2019 jul

Abstract

Cardiac differentiation of human pluripotent stem cells may be induced under chemically defined conditions, wherein the regulation of Wnt/$\beta$-catenin pathway is often desirable. Here, we examined the effect of trolox, a vitamin E analog, on the cardiac differentiation of human embryonic stem cells (hESCs). 6-Hydroxy-2,5,7,8-tetramethylchromane-2-carboxylic acid (Trolox) significantly enhanced cardiac differentiation in a time- and dose-dependent manner after the mesodermal differentiation of hESCs. Trolox promoted hESC cardiac differentiation through its inhibitory activity against the Wnt/$\beta$-catenin pathway. This study demonstrates an efficient cardiac differentiation method and reveals a novel Wnt/$\beta$-catenin regulator.
Single-Cell Gene Expression Analysis of a Human ESC Model of Pancreatic Endocrine Development Reveals Different Paths to $\beta$-Cell Differentiation. M. B. K. Petersen et al. Stem cell reports 2017

Abstract

The production of insulin-producing $\beta$ cells from human embryonic stem cells (hESCs) in vitro represents a promising strategy for a cell-based therapy for type 1 diabetes mellitus. To explore the cellular heterogeneity and temporal progression of endocrine progenitors and their progeny, we performed single-cell qPCR on more than 500 cells across several stages of in vitro differentiation of hESCs and compared them with human islets. We reveal distinct subpopulations along the endocrine differentiation path and an early lineage bifurcation toward either polyhormonal cells or $\beta$-like cells. We uncover several similarities and differences with mouse development and reveal that cells can take multiple paths to the same differentiation state, a principle that could be relevant to other systems. Notably, activation of the key $\beta$-cell transcription factor NKX6.1 can be initiated before or after endocrine commitment. The single-cell temporal resolution we provide can be used to improve the production of functional $\beta$ cells.
Trolox prevents osteoclastogenesis by suppressing RANKL expression and signaling. J.-H. Lee et al. The Journal of biological chemistry 2009 may

Abstract

Excessive receptor activator of NF-kappaB ligand (RANKL) signaling causes enhanced osteoclast formation and bone resorption. Thus, down-regulation of RANKL expression or its downstream signals may be a therapeutic approach to the treatment of pathological bone loss. In this study, we investigated the effects of Trolox, a water-soluble vitamin E analogue, on osteoclastogenesis and RANKL signaling. Trolox potently inhibited interleukin-1-induced osteoclast formation in bone marrow cell-osteoblast coculture by abrogating RANKL induction in osteoblasts. This RANKL reduction was attributed to the reduced production of prostaglandin E(2) via a down-regulation of cyclooxygenase-2 activity. We also found that Trolox inhibited osteoclast formation from bone marrow macrophages induced by macrophage colony-stimulating factor plus RANKL in a reversible manner. Trolox was effective only when present during the early stage of culture, which implies that it targets early osteoclast precursors. Pretreatment with Trolox did not affect RANKL-induced early signaling pathways, including MAPKs, NF-kappaB, and Akt. We found that Trolox down-regulated the induction by RANKL of c-Fos protein by suppressing its translation. Ectopic overexpression of c-Fos rescued the inhibition of osteoclastogenesis by Trolox in bone marrow macrophages. Trolox also suppressed interleukin-1-induced osteoclast formation and bone loss in mouse calvarial bone. Taken together, our findings indicate that Trolox prevents osteoclast formation and bone loss by inhibiting both RANKL induction in osteoblasts and c-Fos expression in osteoclast precursors.