A9481
AD 198
≥98% (HPLC), solid
Synonym(s):
N-Benzyladriamycin-14-valerate
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About This Item
Empirical Formula (Hill Notation):
C39H43NO12
CAS Number:
Molecular Weight:
717.76
UNSPSC Code:
12352200
Pricing and availability is not currently available.
assay
≥98% (HPLC)
form
solid
color
red
solubility
DMSO: >10 mg/mL, H2O: insoluble
storage temp.
2-8°C
SMILES string
CCCCC(=O)OCC(=O)[C@@]1(O)C[C@H](O[C@H]2C[C@H](NCc3ccccc3)[C@H](O)[C@H](C)O2)c4c(O)c5C(=O)c6c(OC)cccc6C(=O)c5c(O)c4C1
Biochem/physiol Actions
AD 198 is a PKC-delta activator.
AD 198 is a PKC-delta activator. Phospholipid scramblase 3 (PLS3) is an enzyme that plays a critical role in mitochondrial morphology, functions, and apoptotic response. During apoptosis, activated protein kinase C-delta (PKC-delta) translocates to mitochondria and phosphorylates PLS3. Used to show that PLS3 is a critical downstream effector of PKC-delta in AD 198-induced apoptosis.
Storage Class
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
ppe
Eyeshields, Gloves, type N95 (US)
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K Kashfi et al.
Biochemical pharmacology, 40(7), 1441-1448 (1990-10-01)
Adriamycin (ADR; doxorubicin) and its highly lipophilic, less toxic analogue N-benzyl-adriamycin-14-valerate (AD 198) were found to inhibit rat heart and liver carnitine palmitoyltransferases of both mitochondrial outer and inner membranes. The outer membrane enzyme was more sensitive to inhibition by
Yongwen He et al.
Cancer research, 65(21), 10016-10023 (2005-11-04)
Phospholipid scramblase 3 (PLS3) is an enzyme that plays a critical role in mitochondrial morphology, functions, and apoptotic response. During apoptosis, activated protein kinase C-delta (PKC-delta) translocates to mitochondria and phosphorylates PLS3. Here, we utilize an extranuclear-targeted anthracycline N-benzyladriamycin-14-valerate (AD198)
Leonard Lothstein et al.
Leukemia research, 31(8), 1085-1095 (2006-12-26)
Bcr-Abl activity in chronic myelogenous leukemia (CML) results in dysregulated cell proliferation and resistance against multiple cytotoxic agents due to the constitutive activation of proliferative signaling pathways. Currently, the most effective treatment of CML is the inhibition of Bcr-Abl activity