PD173074

Tyrosine kinase inhibitor; Inhibits FGFR

PD173074

Tyrosine kinase inhibitor; Inhibits FGFR

From: 417 USD
Catalog #
72162_C
Tyrosine kinase inhibitor; Inhibits FGFR

Overview

PD173074 is a selective and potent, ATP-competitive inhibitor of FGFR. It acts on both FGFR3 and FGFR1 (IC₅₀ = 5 and 21.5 nM respectively), and also inhibits FGFR2, FGFR4 and KDR. It is approximately 1000 times more potent than another common FGFR inhibitor SU5402. (Koziczak et al., Mohammadi et al., Trudel et al.)

REPROGRAMMING
· Prevents excision-mediated differentiation of mouse induced pluripotent stem cells generated using piggyBac transposons (Kaji et al.).
· Promotes reprogramming of human embryonic stem (ES) cells to naïve cells, or their maintenance in a naïve state, in combination with with Oct4, Klf4, and Klf2, LIF, CHIR99021 , and PD0325901. (Hanna et al.)

MAINTENANCE AND SELF-RENEWAL
· Suppresses the differentiation of mouse ES cells and maintains the undifferentiated state (Kunath et al., Ying et al.).

DIFFERENTIATION
· Blocks neural differentiation of mouse ES cells (Stavridis et al.).
· Promotes differentiation of human ES cells, but not when they are in a naïve or "ground" state (Hanna et al.).
Alternative Names
Not applicable
Cell Type
Pluripotent Stem Cells
Species
Human, Mouse, Rat, Non-Human Primate, Other
Application
Differentiation, Maintenance, Reprogramming
Area of Interest
Stem Cell Biology
CAS Number
219580-11-7
Chemical Formula
C₂₈H₄₁N₇O₃
Molecular Weight
523.7 g/mol
Purity
≥ 95%
Pathway
Tyrosine Kinase
Target
FGFR

Scientific Resources

Product 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
PD173074
Catalog #
72164
Lot #
All
Language
English
Document Type
Safety Data Sheet
Product Name
PD173074
Catalog #
72164
Lot #
All
Language
English

Product 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.

Data and Publications

Publications (8)

Human embryonic stem cells with biological and epigenetic characteristics similar to those of mouse ESCs. Hanna J et al. Proceedings of the National Academy of Sciences of the United States of America 2010 MAY

Abstract

Human and mouse embryonic stem cells (ESCs) are derived from blastocyst-stage embryos but have very different biological properties, and molecular analyses suggest that the pluripotent state of human ESCs isolated so far corresponds to that of mouse-derived epiblast stem cells (EpiSCs). Here we rewire the identity of conventional human ESCs into a more immature state that extensively shares defining features with pluripotent mouse ESCs. This was achieved by ectopic induction of Oct4, Klf4, and Klf2 factors combined with LIF and inhibitors of glycogen synthase kinase 3beta (GSK3beta) and mitogen-activated protein kinase (ERK1/2) pathway. Forskolin, a protein kinase A pathway agonist which can induce Klf4 and Klf2 expression, transiently substitutes for the requirement for ectopic transgene expression. In contrast to conventional human ESCs, these epigenetically converted cells have growth properties, an X-chromosome activation state (XaXa), a gene expression profile, and a signaling pathway dependence that are highly similar to those of mouse ESCs. Finally, the same growth conditions allow the derivation of human induced pluripotent stem (iPS) cells with similar properties as mouse iPS cells. The generation of validated naïve" human ESCs will allow the molecular dissection of a previously undefined pluripotent state in humans and may open up new opportunities for patient-specific�
Virus-free induction of pluripotency and subsequent excision of reprogramming factors Kaji K et al. Nature 2009

Abstract

Reprogramming of somatic cells to pluripotency, thereby creating induced pluripotent stem (iPS) cells, promises to transform regenerative medicine. Most instances of direct reprogramming have been achieved by forced expression of defined factors using multiple viral vectors. However, such iPS cells contain a large number of viral vector integrations, any one of which could cause unpredictable genetic dysfunction. Whereas c-Myc is dispensable for reprogramming, complete elimination of the other exogenous factors is also desired because ectopic expression of either Oct4 (also known as Pou5f1) or Klf4 can induce dysplasia. Two transient transfection-reprogramming methods have been published to address this issue. However, the efficiency of both approaches is extremely low, and neither has been applied successfully to human cells so far. Here we show that non-viral transfection of a single multiprotein expression vector, which comprises the coding sequences of c-Myc, Klf4, Oct4 and Sox2 linked with 2A peptides, can reprogram both mouse and human fibroblasts. Moreover, the transgene can be removed once reprogramming has been achieved. iPS cells produced with this non-viral vector show robust expression of pluripotency markers, indicating a reprogrammed state confirmed functionally by in vitro differentiation assays and formation of adult chimaeric mice. When the single-vector reprogramming system was combined with a piggyBac transposon, we succeeded in establishing reprogrammed human cell lines from embryonic fibroblasts with robust expression of pluripotency markers. This system minimizes genome modification in iPS cells and enables complete elimination of exogenous reprogramming factors, efficiently providing iPS cells that are applicable to regenerative medicine, drug screening and the establishment of disease models.
The ground state of embryonic stem cell self-renewal. Ying Q-L et al. Nature 2008 MAY

Abstract

In the three decades since pluripotent mouse embryonic stem (ES) cells were first described they have been derived and maintained by using various empirical combinations of feeder cells, conditioned media, cytokines, growth factors, hormones, fetal calf serum, and serum extracts. Consequently ES-cell self-renewal is generally considered to be dependent on multifactorial stimulation of dedicated transcriptional circuitries, pre-eminent among which is the activation of STAT3 by cytokines (ref. 8). Here we show, however, that extrinsic stimuli are dispensable for the derivation, propagation and pluripotency of ES cells. Self-renewal is enabled by the elimination of differentiation-inducing signalling from mitogen-activated protein kinase. Additional inhibition of glycogen synthase kinase 3 consolidates biosynthetic capacity and suppresses residual differentiation. Complete bypass of cytokine signalling is confirmed by isolating ES cells genetically devoid of STAT3. These findings reveal that ES cells have an innate programme for self-replication that does not require extrinsic instruction. This property may account for their latent tumorigenicity. The delineation of minimal requirements for self-renewal now provides a defined platform for the precise description and dissection of the pluripotent state.

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