Details
Stereochemistry | ACHIRAL |
Molecular Formula | C15H17ClN2O2S |
Molecular Weight | 324.826 |
Optical Activity | NONE |
Defined Stereocenters | 0 / 0 |
E/Z Centers | 0 |
Charge | 0 |
SHOW SMILES / InChI
SMILES
ClC1=CC=CC2=C1C=CC=C2S(=O)(=O)N3CCCNCC3
InChI
InChIKey=OZSMSRIUUDGTEP-UHFFFAOYSA-N
InChI=1S/C15H17ClN2O2S/c16-14-6-1-5-13-12(14)4-2-7-15(13)21(19,20)18-10-3-8-17-9-11-18/h1-2,4-7,17H,3,8-11H2
ML-9 is a selective inhibitor of MYLK and CaMK that acts by delaying MYLK phosphorylation through binding at or near the ATP binding site. This naphthalenesulfonamide derivative has been shown to inhibit insulin-stimulated 2-deoxyglucose transport (IC50 = 27 μM), PP-1 activation in adipocytes, PKA, Akt1 (PKB) and Rsk (S6 kinase). ML-9 was also observed to disrupt microfilament bundles with accompanying decrease in P32 incorporation in rat astrocytes. Carbachol illicited cationic currents were inhibitied with ML-9 (IC50 = 7.8 uM) in HEK293 cells. ML-9 has also demonstrated to inhibit natural killer cell lytic acitivity by regulating microfilament contraction as well as catecholamine secretion in intact and permeabilized chromaffin cells. In addition, agonist-induced Ca2+ entry into endothelial cells was completely abolished in the presence of ML-9. ML-9 was found to be a new type of vascular relaxant. ML-9 produced the relaxation of vascular strips contracted by high K+. The relaxation induced by this
compound was not affected by treatment with adrenergic and
cholinergic blocking agents. Thus, the ML-9-induced relaxation
is not due to a block of membrane receptor-associated
mechanisms; rather it has an effect on more basic and common
events in smooth muscle contraction. Moreover, ML-9
inhibited the Ca2+-induced contraction in chemically skinned
vascular smooth muscle cells, suggesting that ML-9 is not a
“calcium channel blocker.”
Originator
Approval Year
Targets
Primary Target | Pharmacology | Condition | Potency |
---|---|---|---|
3.8 µM [Ki] | |||
Target ID: CHEMBL2094138 Sources: https://www.ncbi.nlm.nih.gov/pubmed/1605572 |
32.0 µM [Ki] | ||
Target ID: CHEMBL2093867 Sources: https://www.ncbi.nlm.nih.gov/pubmed/1605572 |
54.0 µM [Ki] |
Conditions
Condition | Modality | Targets | Highest Phase | Product |
---|---|---|---|---|
Primary | Unknown Approved UseUnknown |
|||
Primary | Unknown Approved UseUnknown |
Sample Use Guides
In Vivo Use Guide
Sources: https://www.ncbi.nlm.nih.gov/pubmed/22529961
Male balb/c mice were assigned randomly to either sham burn (control) or 30% total body surface area (TBSA) full thickness burn without or with intraperitoneal injection of ML-9 (2 mg/kg). Treatment with ML-9 attenuated the burn-caused increase of intestinal permeability, mucosa injury, tight junction protein alterations, and decreased MLC phosphorylation, but not MLCK expression.
Route of Administration:
Intraperitoneal
In Vitro Use Guide
Sources: https://www.ncbi.nlm.nih.gov/pubmed/7680348
ML-9 inhibited insulin stimulation of 2-deoxyglucose transport activity in 3T3-L1 adipocytes by 80% at 100 uM (IC50 = 27 uM) without affecting 2-deoxyglucose transport activity in the basal state. The inhibition was independent of extracellular Ca2+ concentration and almost fully reversible at 40 uM ML-9.
Name | Type | Language | ||
---|---|---|---|---|
|
Common Name | English | ||
|
Systematic Name | English |
Code System | Code | Type | Description | ||
---|---|---|---|---|---|
|
LTJ3F5128V
Created by
admin on Sat Dec 16 08:35:39 GMT 2023 , Edited by admin on Sat Dec 16 08:35:39 GMT 2023
|
PRIMARY | |||
|
DTXSID00149246
Created by
admin on Sat Dec 16 08:35:39 GMT 2023 , Edited by admin on Sat Dec 16 08:35:39 GMT 2023
|
PRIMARY | |||
|
4217
Created by
admin on Sat Dec 16 08:35:39 GMT 2023 , Edited by admin on Sat Dec 16 08:35:39 GMT 2023
|
PRIMARY | |||
|
110448-31-2
Created by
admin on Sat Dec 16 08:35:39 GMT 2023 , Edited by admin on Sat Dec 16 08:35:39 GMT 2023
|
PRIMARY |
ACTIVE MOIETY
SALT/SOLVATE (PARENT)