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Key Documents

Safety Information

SML1754

Sigma-Aldrich

CTX1

≥95% (HPLC)

Synonym(s):

3,6-Diamino-9-acridinecarbonitrile, NSC 363260

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100 MG
CN¥3,558.42
500 MG
CN¥8,707.75

CN¥3,558.42


Available to ship onApril 23, 2025Details



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100 MG
CN¥3,558.42
500 MG
CN¥8,707.75

About This Item

Empirical Formula (Hill Notation):
C14H10N4
CAS Number:
Molecular Weight:
234.26
UNSPSC Code:
12352200
NACRES:
NA.77

CN¥3,558.42


Available to ship onApril 23, 2025Details


Assay

≥95% (HPLC)

form

powder

color

, faint to very dark red

solubility

DMSO: 15 mg/mL, clear

storage temp.

2-8°C

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Show Differences

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SML1605401010SML1406
I-BET762 ≥98% (HPLC)

SML1272

I-BET762

OTX015 ≥98% (HPLC)

SML1605

OTX015

I-BET A cell-permeable benzodiazepine compound that binds the tandem bromodomains of BET (bromodomain and extra terminal domain) family members BRD2 (1-473), BRD3 (1-434), and BRD4 (1-477) with high affinity.

401010

I-BET

assay

≥98% (HPLC)

assay

≥98% (HPLC)

assay

≥98% (HPLC)

assay

≥98% (HPLC)

drug control

regulated under CDSA - not available from Sigma-Aldrich Canada

drug control

-

drug control

-

drug control

-

Quality Level

100

Quality Level

100

Quality Level

100

Quality Level

100

storage temp.

2-8°C

storage temp.

2-8°C

storage temp.

−20°C

storage temp.

2-8°C

solubility

DMSO: 10 mg/mL, clear

solubility

DMSO: 20 mg/mL, clear

solubility

DMSO: 50 mg/mL

solubility

DMSO: 5 mg/mL, clear (warmed)

Biochem/physiol Actions

CTX1 is a potent HdmX inhibitor that overcomes HdmX-mediated p53 repression.
CTX1 is a potent HdmX inhibitor that overcomes HdmX-mediated p53 repression. CTX1 inhibits proliferation and induces apoptosis in number of cancer cell lines. CTX1 inhibits growth of primary human AML in immunodeficient mice.

Pictograms

Exclamation mark

Signal Word

Warning

Hazard Statements

Hazard Classifications

Skin Irrit. 2

Storage Class Code

11 - Combustible Solids

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Regulatory Information

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Goutam Karan et al.
Molecular cancer therapeutics, 15(4), 574-582 (2016-02-18)
Inactivation of the p53 tumor suppressor by mutation or overexpression of negative regulators occurs frequently in cancer. As p53 plays a key role in regulating proliferation or apoptosis in response to DNA-damaging chemotherapies, strategies aimed at reactivating p53 are increasingly

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