Skip to Content
Merck
CN

B2640

DL-Buthionine-(S,R)-sulfoximine

synthetic (organic), ≥98% (TLC), γ-glutamylcysteine synthetase inhibitor, powder

Sign In to View Organizational & Contract Pricing.

Select a Size

About This Item

Linear Formula:
CH3(CH2)3S(O)(=NH)CH2CH2CH(NH2)CO2H
CAS Number:
5072-26-4
Molecular Weight:
222.31
UNSPSC Code:
12161501
PubChem Substance ID:
24278264
NACRES:
NA.77
MDL number:
MFCD00070309
Assay:
≥98% (TLC)
Form:
powder
Quality level:
200

Key Documents

View All Documentation
Technical Service
Need help? Our team of experienced scientists is here for you.
Let Us Assist
Technical Service
Need help? Our team of experienced scientists is here for you.
Let Us Assist

Product Name

DL-Buthionine-(S,R)-sulfoximine,

SMILES string

CCCCS(=N)(=O)CCC(N)C(O)=O

InChI key

KJQFBVYMGADDTQ-UHFFFAOYSA-N

InChI

1S/C8H18N2O3S/c1-2-3-5-14(10,13)6-4-7(9)8(11)12/h7,10H,2-6,9H2,1H3,(H,11,12)

biological source

synthetic (organic)

assay

≥98% (TLC)

form

powder

mp

215 °C (dec.) (lit.)

solubility

water: 50 mg/mL, clear to very slightly hazy, colorless to yellow

storage temp.

2-8°C

Quality Level

200

Looking for similar products? Visit Product Comparison Guide

Related Categories

Application

DL-Buthionine-(S,R)-sulfoximine has also been used:
  • to induce oxidative stress in Starlings
  • to deplete choroidal glutathione (GSH) in two-day-old rat pups
  • to test its inhibitory effect on the enzymes, γ-glutamylcysteine synthetase and trypanothione synthetase (TryS) from T. cruzi

DL-Buthionine-(S,R)-sulfoximine has been used to deplete cellular glutathione levels in retinal ganglion cell 5 (RGC-5) cell line.

Biochem/physiol Actions

Depletes cellular glutathione and downregulates GST level.

Features and Benefits

This compound is a featured product for ADME Tox research. Click here to discover more featured ADME Tox products. Learn more about bioactive small molecules for other areas of research at sigma.com/discover-bsm.

General description

DL-buthionine-SR-sulfoximine (BSO) is an amino acid analogue, which acts as an inhibitor of γ-glutamylcysteine synthetase. BSO increases the sensitivity of Trypanosoma cruzi to antiparasitic drugs, such as nifurtimox or benznidazole.

pictograms

Exclamation mark
GHS07

signalword

Warning

Hazard Classifications

Eye Irrit. 2 - Skin Irrit. 2 - STOT SE 3

target_organs

Respiratory system

Storage Class

11 - Combustible Solids

wgk

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable

ppe

dust mask type N95 (US), Eyeshields, Gloves

Choose from one of the most recent versions:

Certificates of Analysis (COA)

Lot/Batch Number
0000517274
0000517274
0000498015
0000498015
0000443005

Don't see the Right Version?

If you require a particular version, you can look up a specific certificate by the Lot or Batch number.

Search for a COA

Already Own This Product?

Find documentation for the products that you have recently purchased in the Document Library.

Visit the Document Library

Citlali Vázquez et al.
FEBS letters, 591(23), 3881-3894 (2017-11-12)
Buthionine sulfoximine (BSO) induces decreased glutathione (GSH) and trypanothione [T(SH)2 ] pools in trypanosomatids, presumably because only gamma-glutamylcysteine synthetase (γECS) is blocked. However, some BSO effects cannot be explained by exclusive γECS inhibition; therefore, its effect on the T(SH)2 metabolism
Experimental inhibition of a key cellular antioxidant affects vocal communication
Messina S, et al.
Functional Ecology, 1101-1110 (2017)
Matthew M Harper et al.
Experimental eye research, 89(4), 538-548 (2009-06-16)
The purpose of this study was to determine the viability of cell-based delivery of brain-derived neurotrophic factor (BDNF) from genetically modified mesenchymal stem cells (MSCs) for neuroprotection of RGC-5 cells. RGC-5 cells were differentiated with the protein kinase inhibitor staurosporine
Brain-derived neurotrophic factor released from engineered mesenchymal stem cells attenuates glutamate-and hydrogen peroxide-mediated death of staurosporine-differentiated RGC-5 cells
Harper MM, et al.
Experimental Eye Research, 89(4), 538-548 (2009)
Ingrid Kratzer et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 38(14), 3466-3479 (2018-03-07)
Exposure of the developing brain to toxins, drugs, or deleterious endogenous compounds during the perinatal period can trigger alterations in cell division, migration, differentiation, and synaptogenesis, leading to lifelong neurological impairment. The brain is protected by cellular barriers acting through
View All Related Papers

Articles

Discover Bioactive Small Molecules for ADME/Tox

Discover Bioactive Small Molecules for ADME/Tox

Related Content

Product Information Sheet - B2640

Product Information Sheet

Our team of scientists has experience in all areas of research including Life Science, Material Science, Chemical Synthesis, Chromatography, Analytical and many others.

Contact Technical Service