1. PI3K/Akt/mTOR
    Metabolic Enzyme/Protease
    Apoptosis
  2. Akt
    Phosphatase
    Apoptosis
  3. TD52 dihydrochloride

TD52 dihydrochloride 

Cat. No.: HY-135699A Purity: 99.90%
Handling Instructions

TD52 dihydrochloride, an Erlotinib (HY-50896) derivative, is an orally active, potent cancerous inhibitor of protein phosphatase 2A (CIP2A) inhibitor. TD52 dihydrochloride mediates the apoptotic effect in triple-negative breast cancer (TNBC) cells via regulating the CIP2A/PP2A/p-Akt signalling pathway. TD52 dihydrochloride indirectly reduced CIP2A by disturbing Elk1 binding to the CIP2A promoter. TD52 dihydrochloride has less p-EGFR inhibition and has potent anti-cancer activity.

For research use only. We do not sell to patients.

TD52 dihydrochloride Chemical Structure

TD52 dihydrochloride Chemical Structure

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5 mg USD 100 In-stock
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10 mg USD 160 In-stock
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25 mg USD 350 In-stock
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50 mg USD 550 In-stock
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100 mg USD 950 In-stock
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Customer Review

Based on 1 publication(s) in Google Scholar

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Description

TD52 dihydrochloride, an Erlotinib (HY-50896) derivative, is an orally active, potent cancerous inhibitor of protein phosphatase 2A (CIP2A) inhibitor. TD52 dihydrochloride mediates the apoptotic effect in triple-negative breast cancer (TNBC) cells via regulating the CIP2A/PP2A/p-Akt signalling pathway. TD52 dihydrochloride indirectly reduced CIP2A by disturbing Elk1 binding to the CIP2A promoter. TD52 dihydrochloride has less p-EGFR inhibition and has potent anti-cancer activity[1].

In Vitro

TD52 dihydrochloride (2-10 μM; 48 hours) shows anti-proliferative ability and induces differential apoptotic effects in these cell lines[1].
TD52 dihydrochloride (5 μM; 48 hours) has minimal effects on p-EGFR or EGFR expression but downregulated CIP2A expression[1].
TD52 dihydrochloride (2.5, 5, 7.5 μM; 48 hours) time-dependently induces apoptosis accompanied with downregulating CIP2A and p-Akt[1].
TD52 dihydrochloride (5 μM; 24 hours) significantly increases the phosphatase activity of PP2A in TNBC cells[1].
TD52 dihydrochloride (5 μM; 48 hours) has no obvious effects on other common RTKs, such as IGFR, PDGFR and VEGFR2[1].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

In Vivo

TD52 dihydrochloride (10 mg/kg/day; oral gavage; for 52 days) significantly inhibits MDA-MB-468 xenograft tumour size and tumour weight[1].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Molecular Weight

433.33

Formula

C24H18Cl2N4

SMILES

C#CC1=CC(NC2=NC3=CC=CC=C3N=C2NC4=CC=CC(C#C)=C4)=CC=C1.[H]Cl.[H]Cl

Shipping

Room temperature in continental US; may vary elsewhere.

Storage
Powder -20°C 3 years
4°C 2 years
In solvent -80°C 6 months
-20°C 1 month
Solvent & Solubility
In Vitro: 

DMSO : 25 mg/mL (57.69 mM; ultrasonic and warming and heat to 60°C)

Preparing
Stock Solutions
Concentration Solvent Mass 1 mg 5 mg 10 mg
1 mM 2.3077 mL 11.5386 mL 23.0771 mL
5 mM 0.4615 mL 2.3077 mL 4.6154 mL
10 mM 0.2308 mL 1.1539 mL 2.3077 mL
*Please refer to the solubility information to select the appropriate solvent.
Purity & Documentation
References
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Product Name:
TD52 dihydrochloride
Cat. No.:
HY-135699A
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