research use only

MYLS22

Cat.No.S9885

MYLS22 is a first-in-class and selective inhibitor of optic atrophy 1 (OPA1) with anti-angiogenesis and anti-cancer activity.
MYLS22 Chemical Structure

Chemical Structure

Molecular Weight: 443.52

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Quality Control

Batch: Purity: 99.91%
99.91

Solubility

In vitro
Batch:

DMSO : 89 mg/mL (200.66 mM)
(Moisture-contaminated DMSO may reduce solubility. Use fresh, anhydrous DMSO.)

Water : Insoluble

Ethanol : Insoluble

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In vivo
Batch:

In vivo Formulation Calculator (Clear solution)

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Working concentration: mg/ml;

Method for preparing DMSO master liquid: mg drug pre-dissolved in μL DMSO ( Master liquid concentration mg/mL, Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug. )

Method for preparing in vivo formulation: Take μL DMSO master liquid, next addμL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O, mix and clarify.

Method for preparing in vivo formulation: Take μL DMSO master liquid, next add μL Corn oil, mix and clarify.

Note: 1. Please make sure the liquid is clear before adding the next solvent.
2. Be sure to add the solvent(s) in order. You must ensure that the solution obtained, in the previous addition, is a clear solution before proceeding to add the next solvent. Physical methods such
as vortex, ultrasound or hot water bath can be used to aid dissolving.

Chemical Information, Storage & Stability

Molecular Weight 443.52 Formula

C24H21N5O2S

Storage (From the date of receipt) 3 years -20°C powder
CAS No. 306959-01-3 -- Storage of Stock Solutions

Synonyms N/A Smiles CN1N(C(=O)C(=C1C)NC(=O)C2=CC3=C(S2)[N](N=C3C)C4=CC=CC=C4)C5=CC=CC=C5

Mechanism of Action

Targets/IC50/Ki
OPA1
In vitro

Opa1 inhibitor MYLS22 can result in higher maximal and residual cytoplasmic calcium levels, and alter T cell receptor (TCR) signaling in thymocytes with higher susceptibility to apoptosis.

In vivo

MYLS22, a small molecule first-in-kind Opa1-specific inhibitor, can affect angiogenesis, tumor growth and metastasis by impinging on NF-κB activity and on angiogenic gene expression.<sup><a class="sref" href="#s_ref">[1]</a></sup>

References

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