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SML1362

Sigma-Aldrich

L755507

≥98% (HPLC)

Synonym(s):

4-[[(Hexylamino)carbonyl]amino]-N-[4-[2-[[(2S)-2-hydroxy-3-(4-hydroxyphenoxy)propyl]amino]ethyl]phenyl]-benzenesulfonamide, L-755,507

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About This Item

Empirical Formula (Hill Notation):
C30H40N4O6S
CAS Number:
Molecular Weight:
584.73
UNSPSC Code:
12352200
PubChem Substance ID:
NACRES:
NA.77

Quality Level

Assay

≥98% (HPLC)

form

powder

color

white to beige

solubility

DMSO: 20 mg/mL, clear

storage temp.

2-8°C

SMILES string

OC1=CC=C(OC[C@@H](O)CNCCC2=CC=C(NS(C3=CC=C(NC(NCCCCCC)=O)C=C3)(=O)=O)C=C2)C=C1

InChI

1S/C30H40N4O6S/c1-2-3-4-5-19-32-30(37)33-24-10-16-29(17-11-24)41(38,39)34-25-8-6-23(7-9-25)18-20-31-21-27(36)22-40-28-14-12-26(35)13-15-28/h6-17,27,31,34-36H,2-5,18-22H2,1H3,(H2,32,33,37)/t27-/m0/s1

InChI key

NYYJKMXNVNFOFQ-MHZLTWQESA-N

General description

L755507 is a derivative of 4-acylaminobenzenesulfonamide.

Application

L755507 has been shown to enhance CRISPR genome editing efficiency. To see other small molecule CRISPR enhancers, visit sigma.com/CRISPR-enhancers.

Biochem/physiol Actions

L755507 is a potent β3-adrenergic receptor partial agonist with an EC50 value of 0.43 nM for β3 receptors with over 440-fold selectivity for β3 compared to β1 and β2-adrenergic receptor binding. L755507 has been shown to enhance CRISPR-mediated homology-directed repair (HDR) efficiency in human induced pluripotent stem cells (iPSCs), increasing the efficiency of GFP insertion by 3-fold compared to control cells.
L755507 is a potent β3-adrenergic receptor partial agonist.
L755507 is found to stimulate the breakdown of lipids in human adipose tissues. L755507 also promotes urinary bladder relaxation.

Storage Class Code

11 - Combustible Solids

WGK

WGK 3

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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Dana S Hutchinson et al.
British journal of pharmacology, 135(8), 1903-1914 (2002-04-18)
1. This study characterizes the mouse beta(3a)-adrenoceptor (AR) and the splice variant of the beta(3)-AR (beta(3b)-AR) expressed in Chinese hamster ovary cells (CHO-K1). 2. Stable clones with high (approximately 1200), medium (approximately 500) or low receptor expression (approximately 100 fmol
Tools to study β 3-adrenoceptors.
Vrydag W and Michel M C
Naunyn-Schmiedeberg'S Archives of Pharmacology, 374(5-6), 385-398 (2007)
E R Parmee et al.
Bioorganic & medicinal chemistry letters, 8(9), 1107-1112 (1999-01-01)
A study of 4-acylaminobenzenesulfonamides in a cloned human beta 3 adrenergic receptor assay resulted in the discovery of n-hexylurea, L-755,507 (22). This 0.43 nM beta 3 agonist, which is > 440-fold selective over both beta 1 and beta 2 binding
Masaaki Sato et al.
Molecular pharmacology, 74(5), 1417-1428 (2008-08-08)
This study identifies signaling pathways activated by the beta(2)-/beta(3)-adrenoceptor (AR) agonist zinterol, the selective beta(3)-AR agonist L755507, and the selective beta(3)-AR antagonist L748337 in CHO-K1 cells expressing human beta(3)-adrenoceptors. Zinterol and L755507 caused a robust concentration-dependent increase in cAMP accumulation
Chen Yu et al.
Cell stem cell, 16(2), 142-147 (2015-02-07)
The bacterial CRISPR-Cas9 system has emerged as an effective tool for sequence-specific gene knockout through non-homologous end joining (NHEJ), but it remains inefficient for precise editing of genome sequences. Here we develop a reporter-based screening approach for high-throughput identification of

Articles

Modulation of homology-directed repair (HDR) within the context of CRISPR-genome editing has led to the identification of small molecules that enhance CRISPR-mediated HDR efficiency in various cell types.

Modulation of homology-directed repair (HDR) within the context of CRISPR-genome editing has led to the identification of small molecules that enhance CRISPR-mediated HDR efficiency in various cell types.

Modulation of homology-directed repair (HDR) within the context of CRISPR-genome editing has led to the identification of small molecules that enhance CRISPR-mediated HDR efficiency in various cell types.

Modulation of homology-directed repair (HDR) within the context of CRISPR-genome editing has led to the identification of small molecules that enhance CRISPR-mediated HDR efficiency in various cell types.

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