Ac-DEVD-AFC is a fluorogenic substrate (λex=400 nm, λem=530 nm).
体外研究 (In Vitro)
After incubation with Ac-DEVD-AFC for 1 hour, significant increase of caspase-3 activity is observed at 4 hour compare with control. There are no significant increases of caspase-3 activity in Photofrin and LPLI group. The cleavage of Ac-DEVD-AFC in response to caspase-3 activation is remarkably inhibited by shRNA-BimL transfection[1].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
[1]. Wang X, et al. Involvement of Bim in Photofrin-mediated photodynamically induced apoptosis. Cell Physiol Biochem. 2015;35(4):1527-36.
Cell Assay [1]
For the detection of caspase-3 activity, PBS washes cell pellets (derive from either the medium or the adherent cells) which are suspended in extract buffer [25 mM HEPES (pH7.4), 0.1% TritonX-l00, 10% glycerol, 5 mM DTT, 1mM phenylmethylsulfonyl fluoride, 10 mg/mL pepstatin, and 10 mg/mL Leupeptin] and vortexed vigorously. 20μl of extract (corresponding to 10% of the sample) are incubated with the caspase-3 fluorogenic substrates Ac-DEVD-AFC at 100 μM final concentration at room temperature, and caspase-3 activity is measured continuously by monitoring the release of fluorigenic AFC at 37°C[1].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
参考文献
[1]. Wang X, et al. Involvement of Bim in Photofrin-mediated photodynamically induced apoptosis. Cell Physiol Biochem. 2015;35(4):1527-36.
Angstrom6 (A6 Peptide) is an 8 amino-acid peptide derived from single-chain urokinase plasminogen activator (scuPA) and interferes with the uPA/uPAR cascade and abrogates downstream effects. Angstrom6 binds to CD44 resulting in the inhibition of migration, invasion, and metastasis of tumor cells, and the modulation of CD44-mediated cell signaling[1][2].
体外研究 (In Vitro)
Angstrom6 is effective at blocking the migration of the OVCAR8, OVCAR3, ES2, IGROV-1, MDA-MB-468, and MDA-MB361 cells with IC50s in the range of 10 to 100 nM[3]. Angstrom6 potentiates the CD44-dependent adhesion of cancer cells to hyaluronic acid and activated CD44-mediated signaling, as evidenced by focal adhesion kinase and MAP/ERK kinase phosphorylation[3].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究 (In Vivo)
Angstrom6 (100 mg/kg; s.c. twice daily) reduces the number of lung foci generated by the i.v. injection of B16-F10 melanoma cells by 50%[3].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model:
C57Bl/6 mice (bearing B16-F10 cells)[3]
Dosage:
100 mg/kg
Administration:
S.c.; twice a day for 11 days
Result:
Reduced the number of lung nodules and reduced the number of lung metastases to 50% of control.
分子量
910.97
Formula
C39H62N10O15
CAS 号
220334-14-5
Sequence
Ac-Lys-Pro-Ser-Ser-Pro-Pro-Glu-Glu-NH2
Sequence Shortening
Ac-KPSSPPEE-NH2
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Ghamande SA, et al. A phase 2, randomized, double-blind, placebo-controlled trial of clinical activity and safety of subcutaneous A6 in women with asymptomatic CA125 progression after first-line chemotherapy of epithelial ovarian cancer. Gynecol Oncol. 2008;111(1):89-94.
[2]. Finlayson M. Modulation of CD44 Activity by A6-Peptide. Front Immunol. 2015;6:135. Published 2015 Mar 30.
[3]. Piotrowicz RS, et al. A6 peptide activates CD44 adhesive activity, induces FAK and MEK phosphorylation, and inhibits the migration and metastasis of CD44-expressing cells. Mol Cancer Ther. 2011;10(11):2072-2082.
