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Home > products > API Active Pharmaceutical Ingredient > Selinexor CAS 1393477-72-9

Selinexor CAS 1393477-72-9

Product Details

Place of Origin: China

Brand Name: Sunshine

Certification: ISO,COA

Model Number: 1393477-72-9

Payment & Shipping Terms

Minimum Order Quantity: Negotiation

Price: Negotiation

Packaging Details: Aluminum Foil Bag, Drum

Delivery Time: 7-15 days

Payment Terms: T/T, L/C, D/A, Western Union

Supply Ability: TON

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Highlight:
CAS NO::
1393477-72-9
Appearance::
White To Light Yellow Solid
Molecular Formula::
C17H11F6N7O
Molecular Weight::
443.30600
EINECS NO::
NA
MDL NO::
MFCD27987944
CAS NO::
1393477-72-9
Appearance::
White To Light Yellow Solid
Molecular Formula::
C17H11F6N7O
Molecular Weight::
443.30600
EINECS NO::
NA
MDL NO::
MFCD27987944
Selinexor CAS 1393477-72-9

Product Description:

Product Name: Selinexor CAS NO: 1393477-72-9

 

 

 

Synonyms:

UNII-31TZ62FO8F;

KPT-330;

 

 

 

Chemical & Physical Properties:

Appearance: White to light yellow solid

Assay :≥98.0%

Density: 1.55±0.1 g/cm3(Predicted)

Boiling Point: NA

Flash Point: NA

Refractive Index: 1.594

Store Condition: Store at -20℃ for 1 year (powder); in DMSO or other solvent at 2-4℃for two weeks, at -20℃ for six months

Solubility: DMSO89mg/ml (200.76mM)

 

 

 

 

KPT-330, analog of KPT-185, is an orally bioavailable selective CRM1 inhibitor.IC50 value: Target: CRM1in vitro: As the clinical candidate analog of KPT-185, KPT-330 exhibits similar effects on the viability of T-ALL cells and elicits rapid apoptotic response. KPT-330 also reduces cell growth in MOLT-4, Jurkat, HBP-ALL, KOPTK-1, SKW-3, and DND-41 cell lines, with IC50 values of 34-203 nM [1]. in vivo: KPT-330 dramatically suppresses the growth of T-ALL cells (MOLT-4) and AML cells (MV4–11) in vivo, with little toxicity to normal haematopoietic cells [1]. In SCID mice with diffuse human MM bone lesions, KPT-330 inhibits MM-induced bone lysis and prolongs survival. Moreover, KPT-330 directly impairs osteoclastogenesis and bone resorption by blocking RANKL-induced NF-κB and NFATc1, with minimal impact on osteoblasts and BMSCs [2].

 

 

 

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