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681671

Sigma-Aldrich

IWP-2

≥97% (HPLC), solid, Wnt antagonist, Calbiochem

Synonym(s):

Wnt Antagonist II, IWP-2, Inhibitor of Wnt Production-2, Wnt Pathway Inhibitor II, Porcn Inhibitor I

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About This Item

Empirical Formula (Hill Notation):
C22H18N4O2S3
CAS Number:
Molecular Weight:
466.60
MDL number:
UNSPSC Code:
12352200
NACRES:
NA.77

product name

Wnt Antagonist II, IWP-2, The Wnt Antagonist II, IWP-2, also referenced under CAS 686770-61-6, controls the biological activity of Wnt. This small molecule/inhibitor is primarily used for Cancer applications.

Quality Level

Assay

≥97% (HPLC)

form

solid

manufacturer/tradename

Calbiochem®

storage condition

OK to freeze
protect from light

color

off-white

solubility

DMSO: 2.5 mg/mL

shipped in

ambient

storage temp.

2-8°C

InChI

1S/C22H18N4O2S3/c1-13-7-8-15-17(11-13)31-21(23-15)25-18(27)12-30-22-24-16-9-10-29-19(16)20(28)26(22)14-5-3-2-4-6-14/h2-8,11H,9-10,12H2,1H3,(H,23,25,27)

InChI key

WRKPZSMRWPJJDH-UHFFFAOYSA-N

General description

A cell-permeable benzothiazolyl-acetamide compound that inhibits the cellular Wnt processing and secretion via selective blockage of MBOAT (membrane-bound O-acyltranferase) family member Porcn- (Porcupine) mediated Wnt palmitoylation. IWP-2 does not affect Wnt/β-catenin signaling pathway in general and, unlike IWR-1-endo (Cat. No. 681669), displays no effect against Wnt-stimulated cellular responses. Also available as a 10 mM solution in DMSO (Cat. No. 506072).
A cell-permeable benzothiazolyl-acetamide compound that inhibits the cellular Wnt processing and secretion via selective blockage of MBOAT (membrane-bound O-acyltranferase) family member Porcn- (Porcupine) mediated Wnt palmitoylation. IWP-2 does not affect Wnt/β-catenin signaling pathway in general and, unlike IWR-1-endo (Cat. No. 681669), displays no effect against Wnt-stimulated cellular responses.

Packaging

Packaged under inert gas

Warning

Toxicity: Harmful (C)

Reconstitution

Following reconstitution, aliquot and freeze (-20°C). Stock solutions are stable for up to 3 months at -20°C.

Other Notes

Chen, B., et al. 2009. Nature Chem. Biol.5, 100.

Legal Information

CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany

Storage Class Code

11 - Combustible Solids

WGK

WGK 2

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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Generation of cardiomyocytes from human pluripotent stem cells (hPSCs) is of high interest for disease modelling and regenerative medicine. hPSCs can provide an unlimited source of patient-specific cardiomyocytes that are otherwise difficult to obtain from individuals. Moreover, the low proliferation
Alex Neagu et al.
Nature cell biology, 22(5), 534-545 (2020-05-06)
Following implantation, the naive pluripotent epiblast of the mouse blastocyst generates a rosette, undergoes lumenogenesis and forms the primed pluripotent egg cylinder, which is able to generate the embryonic tissues. How pluripotency progression and morphogenesis are linked and whether intermediate
Jeffrey Aalders et al.
Matrix biology : journal of the International Society for Matrix Biology, 126, 14-24 (2024-01-16)
Pathogenic variants in the FBN1 gene, which encodes the extracellular matrix protein fibrillin-1, cause Marfan syndrome (MFS), which affects multiple organ systems, including the cardiovascular system. Myocardial dysfunction has been observed in a subset of patients with MFS and in
Yuan Gao et al.
Journal of pain research, 13, 1049-1058 (2020-06-18)
The upregulation of spinal NMDA receptor is a crucial mechanism in remifentanil-induced hyperalgesia (RIH). Wnt3a/β-catenin pathway plays an important role in neuropathic pain. We hypothesized that wnt3a inhibitor (iwp-2) could downregulate the expression of NR2B subunit in NMDA receptor, in
Cornelis J Boogerd et al.
Nature communications, 14(1), 4716-4716 (2023-08-06)
The inability of adult human cardiomyocytes to proliferate is an obstacle to efficient cardiac regeneration after injury. Understanding the mechanisms that drive postnatal cardiomyocytes to switch to a non-regenerative state is therefore of great significance. Here we show that Arid1a

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