Rolipram

cAMP pathway activator; Inhibits type 4 cyclic nucleotide phosphodiesterases (PDE4)

Rolipram

cAMP pathway activator; Inhibits type 4 cyclic nucleotide phosphodiesterases (PDE4)

From: 40 USD
Catalog #
73382_C
cAMP pathway activator; Inhibits type 4 cyclic nucleotide phosphodiesterases (PDE4)

Overview

Rolipram is a cell-permeable, selective inhibitor of Type 4 cyclic nucleotide phosphodiesterases (PDE4), which mediate cyclic AMP (cAMP) degradation. Rolipram preferably inhibits PDE4 isoform A (IC₅₀ = 3 nM) over other isoforms such as B and D (IC₅₀ = 130 and 240 nM respectively; MacKenzie & Houslay). It inhibits interferon (IFN)-γ stimulated phosphorylation of p38 mitogen-activated protein (MAP) kinase through PDE4B and/or PDE4D isoform inhibition (MacKenzie & Houslay).

DIFFERENTIATION
· Enhances osteoblastic differentiation of mouse mesenchymal stem cells (MSCs) induced by BMP-2 (Munisso et al.)
· Induces neural differentiation of human bone marrow-derived MSCs (Alexanian et al.)

REPROGRAMMING
· Induces reprogramming of adult human dermal fibroblasts (AHDFs) into induced neuronal stem cells, in combination with A83-01, CHIR99021, sodium butyrate, LPA, SP600125, and exogenous OCT4 expression (Zhu et al.)

DISEASE MODELING
· Promotes survival of newly formed mouse hippocampal neurons in a mouse model of ischemia (Sasaki et al.)
· Reverses amphetamine-induced reductions in auditory-evoked potentials in a C57BL/6J mouse model of schizophrenia (Maxwell et al.)

IMMUNOLOGY
· Inhibits inflammation by suppressing leukocyte function, inhibiting C5a-stimulated leukotriene C4 (LTC4) synthesis in human eosinophils (Tenor et al.)
· Inhibits lipopolysaccharide (LPS)-induced tumor necrosis factor (TNF) synthesis in human monocytes (Souness et al.)
Alternative Names
SB 95952; ZK 62711
Cell Type
Mesenchymal Stem and Progenitor Cells, Monocytes, Neural Stem and Progenitor Cells, Neurons, Osteoblasts
Species
Human, Mouse, Rat, Non-Human Primate, Other
Application
Differentiation, Reprogramming
Area of Interest
Disease Modeling, Immunology, Stem Cell Biology
CAS Number
61413-54-5
Chemical Formula
C₁₆H₂₁NO₃
Molecular Weight
275.3 g/mol
Purity
≥ 98%
Pathway
cAMP
Target
PDE

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
Rolipram
Catalog #
73382, 73384
Lot #
All
Language
English
Document Type
Safety Data Sheet
Product Name
Rolipram
Catalog #
73382, 73384
Lot #
All
Language
English

Applications

This product is designed for use in the following research area(s) as part of the highlighted workflow stage(s). Explore these workflows to learn more about the other products we offer to support each research area.

Resources and Publications

Publications (8)

Small molecules enable OCT4-mediated direct reprogramming into expandable human neural stem cells. Zhu S et al. Cell research 2014
Cilomilast enhances osteoblast differentiation of mesenchymal stem cells and bone formation induced by bone morphogenetic protein 2. Munisso MC et al. Biochimie 2012

Abstract

A rapid and efficient method to stimulate bone regeneration would be useful in orthopaedic stem cell therapies. Rolipram is an inhibitor of phosphodiesterase 4 (PDE4), which mediates cyclic adenosine monophosphate (cAMP) degradation. Systemic injection of rolipram enhances osteogenesis induced by bone morphogenetic protein 2 (BMP-2) in mice. However, there is little data on the precise mechanism, by which the PDE4 inhibitor regulates osteoblast gene expression. In this study, we investigated the combined ability of BMP-2 and cilomilast, a second-generation PDE4 inhibitor, to enhance the osteoblastic differentiation of mesenchymal stem cells (MSCs). The alkaline phosphatase (ALP) activity of MSCs treated with PDE4 inhibitor (cilomilast or rolipram), BMP-2, and/or H89 was compared with the ALP activity of MSCs differentiated only by osteogenic medium (OM). Moreover, expression of Runx2, osterix, and osteocalcin was quantified using real-time polymerase chain reaction (RT-PCR). It was found that cilomilast enhances the osteoblastic differentiation of MSCs equally well as rolipram in primary cultured MSCs. Moreover, according to the H89 inhibition experiments, Smad pathway was found to be an important signal transduction pathway in mediating the osteogenic effect of BMP-2, and this effect is intensified by an increase in cAMP levels induced by PDE4 inhibitor.
Transplanted neurally modified bone marrow-derived mesenchymal stem cells promote tissue protection and locomotor recovery in spinal cord injured rats. Alexanian AR et al. Neurorehabilitation and neural repair 2011

Abstract

BACKGROUND: Stem cell-based therapy for repair and replacement of lost neural cells is a promising treatment for central nervous system (CNS) diseases. Bone marrow (BM)-derived mesenchymal stem cells (MSCs) can differentiate into neural phenotypes and be isolated and expanded for autotransplantation with no risk of rejection. OBJECTIVE: The authors examined whether transplanted neurally induced human MSCs (NI hMSCs), developed by a new procedure, can survive, differentiate, and promote tissue protection and functional recovery in injured spinal cord (ISC) rats. METHODS: Neural induction was achieved by exposing cells simultaneously to inhibitors of DNA methylation, histone deacetylation, and pharmacological agents that increased cAMP levels. Three groups of adult female Sprague-Dawley rats were injected immediately rostral and caudal to the midline lesion with phosphate-buffered saline, MSCs, or NI hMSCs, 1 week after a spinal cord impact injury at T-8. Functional outcome was measured using the Basso Beattie Bresnahan (BBB) locomotor rating scale and thermal sensitivity test on a weekly basis up to 12 weeks postinjury. Graft integration and anatomy of spinal cord was assessed by stereological, histochemical, and immunohistochemical techniques. RESULTS: The transplanted NI hMSCs survived, differentiated, and significantly improved locomotor recovery of ISC rats. Transplantation also reduced the volume of lesion cavity and white matter loss. CONCLUSION: This method of hMSC modification may provide an alternative source of autologous adult stem cells for CNS repair.

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