MSDH
(Synonyms: O-Methyl-serine dodecylamide hydrochloride)
MSDH (O-Methyl-serine dodecylamide hydrochloride) is a lysosomotropic detergent that targets the lysosomal membrane. MSDH enters cells via endocytosis, accumulates in lysosomes and becomes protonated, forming physiological pH vesicles that dissociate at acidic pH, and acts as a micellar detergent. MSDH induces lysosomal membrane permeabilization, deacidification, release of cathepsin D/B and β-N-acetylglucosaminidase, and translocation of galectins to lysosomes. MSDH induces apoptosis, necrosis, caspase-3 activation, a decrease in mitochondrial transmembrane potential, and elevated p62/LC3BII levels. MSDH can be used in research on non-alcoholic steatohepatitis and head and neck squamous cell carcinoma.
Nur für Forschungszwecke. Wir verkaufen nicht an Patienten.
- CAS. Nr.: 2074614-60-9
- Formel: C16H35ClN2O2
- Molecular Weight:322.92
-
Speicherung:
Please store the product under the recommended conditions in the Certificate of Analysis.
Größe
Preis
Verfügbarkeit
Menge
Amount: USD 0.00
Please select quantity
or
or
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
-
Biologische Aktivität
-
Chemical Information
- Protokoll
- Reinheit & Dokumentation
- Verweise
-
Help & FAQs
Alle Cathepsin Isoform-spezifische Produkte anzeigen
MoreAlle Caspase Isoform-spezifische Produkte anzeigen
More
Biologische Aktivität
Beschreibung
MSDH (O-Methyl-serine dodecylamide hydrochloride) is a lysosomotropic detergent that targets the lysosomal membrane. MSDH enters cells via endocytosis, accumulates in lysosomes and becomes protonated, forming physiological pH vesicles that dissociate at acidic pH, and acts as a micellar detergent. MSDH induces lysosomal membrane permeabilization, deacidification, release of cathepsin D/B and β-N-acetylglucosaminidase, and translocation of galectins to lysosomes. MSDH induces apoptosis, necrosis, caspase-3 activation, a decrease in mitochondrial transmembrane potential, and elevated p62/LC3BII levels. MSDH can be used in research on non-alcoholic steatohepatitis and head and neck squamous cell carcinoma[1][2][3][4][5][6][7][8][9].
|
Cathepsin D |
Cathepsin B |
Caspase-3 |
p62 |
LC3BII |
Cellular Effect
|
Cell Line
|
Type | Value | Description | References |
|---|---|---|---|---|
| MIA PaCa-2 | IC50 |
55.5 μM
|
Cell viability inhibition against human MIA PaCa-2 cells assessed as reduction in viability incubated 24 hrs by MTS assay measuring OD at 490 nm.
Cell viability inhibition against human MIA PaCa-2 cells assessed as reduction in viability incubated 24 hrs by MTS assay measuring OD at 490 nm.
|
32934241 |
| HT-29 | IC50 |
30.3 μM
|
Cell viability inhibition against human HT29 cells assessed as reduction in viability incubated 24 hrs by MTS assay measuring OD at 490 nm.
Cell viability inhibition against human HT29 cells assessed as reduction in viability incubated 24 hrs by MTS assay measuring OD at 490 nm.
|
32934241 |
In Vitro
Anti-cancerApoptosisLysosomal MetabolismAutophagyLipid MetabolismOxidative StressInnate ImmunityMitochondrial Function
Anti-cancer
MSDH (24-48 h) inhibits MIA PaCa-2 and HT29 cell viability with 24 h IC50 values of 55.5 and 30.3 µM and 48 h IC values of 51.1 and 20.0 µM, respectively[5].
Anti-cancer
Apoptosis
Lysosomal Metabolism
MSDH (20 mM; 48 h after seeding) in UT-SCC-77 head and neck squamous cell carcinoma cells induces apoptosis and causes limited LAMP-2 translocation into digitonin-extractable cytosol[2].
Apoptosis
MSDH (0-40 µM; 1-8 h) induces plasma membrane damage at ≥30 µM, viability loss at ≥10 µM, and caspase-3 activation at 15 µM in human fibroblasts AG1518[8].
MSDH (15 μM; 24 h) induces caspase-3-dependent apoptosis in human foreskin fibroblasts, and lysosomal cholesterol accumulation increases survival from 17% to 100% after 24 h exposure[9].
MSDH (15 μM; 24 h) induces caspase-3-dependent apoptosis in human foreskin fibroblasts, and lysosomal cholesterol accumulation increases survival from 17% to 100% after 24 h exposure[9].
Apoptosis
Autophagy
Lipid Metabolism
Lysosomal Metabolism
MSDH (0-25 μM; 6-12 h) induces LMP-mediated cell death in ASMase+/+ primary mouse hepatocytes, whereas ASMase-/- PMH and HCD-fed PMH are resistant, an effect reversed by 25-hydroxycholesterol[1].
Apoptosis
Lysosomal Metabolism
Lipid Metabolism
MSDH (10-15 mM; 24 h) induces lysosome-dependent apoptosis in human fibroblasts, and cellular sensitivity is inversely related to lysosomal cholesterol content, with NPC1-mutant fibroblasts being less sensitive than wild-type fibroblasts[4].
MSDH (10-15 mM; 24 h) induces cell death in primary rat cortical neurons, and U18666A-induced lysosomal cholesterol accumulation protects these neurons from MSDH-induced apoptosis[4].
MSDH (10-15 mM; 24 h) induces cell death in primary rat cortical neurons, and U18666A-induced lysosomal cholesterol accumulation protects these neurons from MSDH-induced apoptosis[4].
Apoptosis
Oxidative Stress
Innate Immunity
Apoptosis
Autophagy
Lysosomal Metabolism
Innate Immunity
Mitochondrial Function
Apoptosis
MSDH (50 µM; 3-5 h) causes mitochondrial destabilization (decreased Rh-123 fluorescence) only after significant lysosomal rupture in J-774, U937, and THP-1 cells, when about 25-35% of cells are apoptotic[7].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Apoptosis Analysis[2]
-
Cell Line:UT-SCC-77 head and neck squamous cell carcinoma cells
-
Concentration:20 μM
-
Incubation Time:48 h after seeding
-
Result:Induced apoptosis/nuclear fragmentation; cell death was significantly enhanced when cells were treated with TSA (Trichostatin A) (HY-15144) in combination.
Resulted in only a small amount of LAMP-2 protein in the Digitonin (HY-N4000)-extracted cytosolic fraction, similar to STS (Staurosporine) (HY-15141), whereas Cisplatin (HY-17394) caused a more pronounced loss of LAMP-2 from the membrane fraction.
Cells with lower lysosomal pH were more sensitive to apoptosis.
Apoptosis Analysis[4]
-
Cell Line:Human fibroblasts: wild-type (GM05659) and NPC1-mutant (GM18436)
-
Concentration:10-15 μM
-
Incubation Time:24 h
-
Result:Induced a substantial loss of viability in wild-type fibroblasts, whereas NPC1-mutant fibroblasts were less sensitive.
Preincubation of wild-type fibroblasts with U18666A or Quinacrine (HY-13735) prior to exposure significantly decreased sensitivity to apoptosis induction.
Cholesterol reduction in NPC1-mutant fibroblasts by MβCD or 25-HC (25-Hydroxy cholestero) pretreatment increased sensitivity to cell death.
Myriocin (HY-N6798) application did not change sensitivity to apoptosis.
MTT viability results were verified by caspase-3 activity measurement and crystal violet staining.
Apoptosis Analysis[6]
-
Cell Line:human skin fibroblasts (GM00498)
-
Concentration:45 µM
-
Incubation Time:42 h
-
Result:Induced apoptosis at 45 µM for 42 h.
HPβCD-treated healthy cells, LF-loaded cells, and HPβCD-treated LF-loaded cells showed increased resistance relative to untreated controls.
Apoptosis Analysis[7]
-
Cell Line:J-774 cells
-
Concentration:50 µM (3 h and 5 h); 7.5-25 µM (24 h); >75 µM; 50 µM (5 h for electron microscopy)
-
Incubation Time:3 h and 5 h; 24 h; 5 h for electron microscopy
-
Result:At 50 µM, about 15% and 25% of J-774 cells no longer excluded trypan blue after 3 and 5 h, respectively.
At those time points, the frequency of cells with pycnotic apoptotic nuclei was about 25% and 35%, respectively.
Apoptosis was clearly evident after 24 h exposure to 7.5-25 µM, as shown by Wright-Giemsa and TUNEL images in Fig. 2A-C (img-p2-b2-1), or after 3-5 h exposure to 50 µM (data not shown).
Exposure to higher concentrations (>75 µM) caused rapid necrosis without intervening apoptosis.
Electron microscopy after 50 µM for 5 h showed obvious alterations in the acidic vacuolar apparatus indicative of reparative autophagocytosis; lysosomes were plentiful and enlarged with membranous myelin-type inclusions, and many cells showed chromatin margination, nuclear pyknosis, and fragmentation.
Cell Cytotoxicity Assay[8]
-
Cell Line:Human fibroblasts AG1518
-
Concentration:0, 10, 20, 30, 40 µM (LDH); 0, 5, 10, 15, 20 µM (MTT); 15 µM (caspase-3)
-
Incubation Time:1, 2, 4 h (LDH); 1, 2, 4 h (MTT); 0, 2, 4, 8 h (caspase-3)
-
Result:The plasma membrane was intact at concentrations ≤20 µM, while concentrations ≥30 µM caused substantial and rapid plasma membrane damage.
Concentration-dependent loss of viability occurred at concentrations ≥10 µM, and cell death never exceeded 50% with the tested concentrations.
Caspase-3 activity showed a time-dependent increase after exposure to 15 µM.
Chemical Information
-
CAS. Nr. 2074614-60-9
-
Molecular Weight 322.92
-
Formel C16H35ClN2O2
-
SMILES
C(NCCCCCCCCCCCC)([C@H](COC)N)=O.Cl
-
Synonyms
O-Methyl-serine dodecylamide hydrochloride
-
Versand
Room temperature in continental US; may vary elsewhere.
-
Speicherung
Please store the product under the recommended conditions in the Certificate of Analysis.
Reinheit & Dokumentation
Select Batch:
Reinheit:
99.98%
Assay:
99.98%
ee.:
99.98%
Verweise
View More
Calculators
Molaritätsrechner
Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)
=
×
×
Verdünnungsrechner
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)
MSDH Related Classifications
HY-131595 Related Classifications
Powered by Bioz
Keywords
- MSDH
- 2074614-60-9
- O-Methyl-serine dodecylamide
- Biochemical Assay Reagents
- Cathepsin
- Apoptosis
- Caspase
- p62
- Sequestosome-1
- SQSTM1
- apoptosis
- caspase-3
- cathepsin B
- cathepsin D
- head and neck squamous cell carcinoma
- lysosomal cholesterol
- lysosomal membrane permeabilization
- lysosomotropic detergent
- necrosis
- non-alcoholic steatohepatitis
- Inhibitor
- inhibitor
- inhibit