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SML3723

Sigma-Aldrich

JNJ-26854165

≥98% (HPLC)

Synonym(s):

1-N-[2-(1H-Indol-3-yl)ethyl]-4-N-pyridin-4-ylbenzene-1,4-diamine, JNJ 1, JNJ 26854165, N1-[2-(1H-Indol-3-yl)ethyl]-N4-4-pyridinyl-1,4-benzenediamine, Serdemetan

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About This Item

Empirical Formula (Hill Notation):
C21H20N4
CAS Number:
881202-45-5
Molecular Weight:
328.41
MDL number:
MFCD16620518
UNSPSC Code:
12352200
NACRES:
NA.77

Quality Level

100

Assay

≥98% (HPLC)

form

powder

color

white to beige

solubility

DMSO: 2 mg/mL, clear

storage temp.

2-8°C

Biochem/physiol Actions

JNJ-26854165 (serdemetan) is an inhibitor of the E3 ligase human double minute-2 (HDM2) that inhibits cell proliferation and induces apoptosis in models of acute myeloid and lymphoid leukemias, and solid tumors. Also JNJ-26854165 inhibits cholesterol transport. JNJ-26854165 appears to stimulate cholesterol regulatory genes, but simultaneously inhibits cholesterol transport.

Storage Class Code

11 - Combustible Solids

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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The novel anticancer agent JNJ-26854165 induces cell death through inhibition of cholesterol transport and degradation of ABCA1
Journal of Pharmacology and Experimental Therapeutics, 346(3), 381-392 (2013)
Liangshun You et al.
Oncotarget, 8(5), 7777-7790 (2016-12-22)
Chronic myeloid leukemia (CML) is a clonal malignant disease caused by the expression of BCR/ABL. MDM2 (human homolog of the murine double minute-2) inhibitors such as Nutlin-3 have been shown to induce apoptosis in a p53-dependent manner in CML cells
Zih-Yin Lai et al.
International journal of molecular sciences, 22(16) (2021-08-28)
As the most common gene mutation found in cancers, p53 mutations are detected in up to 96% of high-grade serous ovarian carcinoma (HGSOC). Meanwhile, mutant p53 overexpression is known to drive oncogenic phenotypes in cancer patients and to sustain the

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