572924-54-0 Usage
Description
Ridaforolimus (Deforolimus, MK-8669, AP23573) is a semisynthetic derivative of sirolimus, which has been modified to increase its water solubility and amenable to oral or intravenous administration. It is a selective mTOR inhibitor with an IC50 of 0.2 nM in the HT-1080 cell line. Ridaforolimus, formerly known as Deforolimus, acts as a regulator of protein synthesis, cell proliferation, cell cycle progression, and cell survival by binding to the receptor protein FKBP12, forming a complex that inhibits mTORC1 kinase activity. It is currently in Phase 3 of development and has been extensively cited in the literature with over 70 citations.
Uses
Used in Pharmaceutical Industry:
Ridaforolimus (Deforolimus, MK-8669) is used as an immunosuppressant for regulating protein synthesis, cell proliferation, cell cycle progression, and cell survival. It is particularly effective as a potent mTORC1 inhibitor, making it a promising candidate for cancer treatments.
Used in Cancer Treatments:
Ridaforolimus (Deforolimus, MK-8669) is used as a cancer treatment agent, specifically for advanced kidney cancer and other malignancies. It has shown promise in combination with other chemotherapeutic compounds, enhancing the effectiveness of treatments and potentially overcoming resistance in some cases.
Used in Drug Formulation:
Ridaforolimus (Deforolimus, MK-8669) is used in the development of drug formulations containing rapalogs, which have potential against a subset of cancers. Its increased water solubility compared to rapamycin allows for more versatile administration methods, such as oral or intravenous, improving the drug's bioavailability and therapeutic outcomes.
Mechanism of action
Ridaforolimus (also known as AP23573 and MK-8669; formerly known as deforolimus) is an investigational targeted and small-molecule inhibitor of the protein mTOR, a protein that acts as a central regulator of protein synthesis, cell proliferation, cell cycle progression and cell survival, integrating signals from proteins, such as PI3K, AKT and PTEN known to be important to malignancy. Blocking mTOR creates a starvation-like effect in cancer cells by interfering with cell growth, division, metabolism, and angiogenesis.
in vivo
mice bearing mcf7 (breast), pc-3 (prostate), a549 (lung), hct-116 (colon) or panc-1 (pancreas) xenografts have revealed the antitumor efficacy of ridaforolimus [1].
references
[1] rivera vm1, squillace rm, miller d, berk l, wardwell sd, ning y, pollock r, narasimhan ni, iuliucci jd, wang f, clackson t.ridaforolimus (ap23573; mk-8669), a potent mtor inhibitor, has broad antitumor activity and can be optimally administered using intermittent dosing regimens. mol cancer ther. 2011 jun;10(6):1059-71.
Check Digit Verification of cas no
The CAS Registry Mumber 572924-54-0 includes 9 digits separated into 3 groups by hyphens. The first part of the number,starting from the left, has 6 digits, 5,7,2,9,2 and 4 respectively; the second part has 2 digits, 5 and 4 respectively.
Calculate Digit Verification of CAS Registry Number 572924-54:
(8*5)+(7*7)+(6*2)+(5*9)+(4*2)+(3*4)+(2*5)+(1*4)=180
180 % 10 = 0
So 572924-54-0 is a valid CAS Registry Number.
InChI:InChI=1/C53H84NO14P/c1-32-18-14-13-15-19-33(2)44(63-8)30-40-23-21-38(7)53(61,67-40)50(58)51(59)54-25-17-16-20-41(54)52(60)66-45(35(4)28-39-22-24-43(46(29-39)64-9)68-69(11,12)62)31-42(55)34(3)27-37(6)48(57)49(65-10)47(56)36(5)26-32/h13-15,18-19,27,32,34-36,38-41,43-46,48-49,57,61H,16-17,20-26,28-31H2,1-12H3/b15-13+,18-14+,33-19+,37-27+/t32-,34-,35-,36-,38-,39+,40+,41+,43-,44+,45+,46-,48-,49+,53-/m1/s1
572924-54-0Relevant articles and documents
METHOD FOR PREPARING 42-(DIMETHYLPHOSPHINATE) RAPAMYCIN
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, (2014/03/24)
A method for preparing 42-(dimethylphosphinate) Rapamycin (Ridaforolimus) (I) is provided, which has advantages of high conversion rate and no 31,42-bis(dimethyl phosphinate) Rapamycin (III) generated. In the method of the present invention, Rapamycin (II) is firstly reacted with triethyl chlorosilane in a base condition to form 31,42-bis(triethylsilylether) Rapamycin (IV-b), followed by a selective deprotection process to obtain 31-triethylsilylether Rapamycin (V-b). Next, a phosphorylation reaction is performed by using dimethylphosphinic chloride under a base solution to obtain a crude product. Finally, a deprotection reaction is performed in a diluted sulfuric acid solution to obtain a crude product of Ridaforolimus (I). Since the conversion rate of each step of the method of the present invention is higher than 98%, it indicates that the method of the present invention is suitable for industrial production.
