- Product Details
Keywords
- 58066-85-6
- Miltefosine
- 99% purity
Quick Details
- ProName: Miltefosine
- CasNo: 58066-85-6
- Molecular Formula: C21H46NO4P
- Appearance: Crystalline Powder
- Application: intermediate
- DeliveryTime: in stock
- PackAge: According to the need of packing
- Port: Shanghai
- ProductionCapacity: 100 Kilogram/Month
- Purity: 99% purity
- Storage: room temp
- Transportation: air,sea,courier
- LimitNum: 1 Gram
Superiority
Product Name: Miltefosine
Synonyms: 2-(((hexadecyloxy)hydroxyphosphinyl)oxy)-n,n,n-trimethyl-ethanaminiuhydrox;2-(((hexadecyloxy)hydroxyphosphinyl)oxy)-n,n,n-trimethylethanaminiumhydroxid;cholinephosphate,hexadecylester,hydroxide,innersalt;d18506;Hexadecyl 2-(trimethylamino)ethyl phosphate;Miltex;13-18506;2-[[(Hexadecyloxy)hydroxyphasphinyl]oxy]-N,N,N-trimethylethanaminiminner salt
CAS: 58066-85-6
MF: C21H46NO4P
MW: 407.57
EINECS: 622-572-6
Product Categories: Inhibitors;Anti-cancer&immunity;Anti-virals;Intermediates & Fine Chemicals;Pharmaceuticals;Protein Kinase Inhibitors and Activators;Miscellaneous Natural Products;MILTEX;inhibitor
Mol File: 58066-85-6.mol
Details
Melting point 232-234° (dec)
storage temp. room temp
solubility H2O: soluble10mg/mL, clear, colorless
form Crystalline solid
InChIKey PQLXHQMOHUQAKB-UHFFFAOYSA-N
CAS DataBase Reference 58066-85-6(CAS DataBase Reference)
Safety Information
Hazard Codes Xn
Risk Statements 22-43
Safety Statements 36/37
RIDADR UN 2811 6.1 / PGIII
WGK Germany 3
RTECS KH2890000
Toxicity LD50 in rats (mg/kg): 246 orally (Muschiol)
Description Miltefosin, representing the prototype of a new phospholipid structure, was introduced for the palliative treatment of skin metastases in patients with breast cancer. It is highly active against the human leukemia tumor cells xenograft in nude mice, leading to growth inhibition and regression of large established tumors. Its mode of antitumor activity is not mediated by the host immune system but by its pharmacological effects at the level of the cancer cell membrane, distinctly different from that of the classical cytostatic drugs which interact with cell proliferation at the level of DNA replication. Protein kinase C inhibition has been suggested as a possible mechanism.