1. Cell Cycle/DNA Damage
    Autophagy
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  2. Topoisomerase
    Autophagy
    Bacterial
    Antibiotic
  3. Pirarubicin Hydrochloride

Pirarubicin Hydrochloride (Synonyms: THP Hydrochloride)

Cat. No.: HY-13725A Purity: 98.51%
Handling Instructions

Pirarubicin Hydrochloride is an anthracycline antibiotics, acts as a topoisomerase II inhibitor, and is a widely used for treatment of various cancers, in particular, solid tumors.

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

Pirarubicin Hydrochloride Chemical Structure

Pirarubicin Hydrochloride Chemical Structure

CAS No. : 95343-20-7

Size Price Stock Quantity
Solution
10 mM * 1 mL in DMSO USD 66 In-stock
Estimated Time of Arrival: December 31
Solid + Solvent
10 mM * 1 mL
ready for reconstitution
USD 66 In-stock
Estimated Time of Arrival: December 31
Solid
10 mg USD 60 In-stock
Estimated Time of Arrival: December 31
50 mg USD 240 In-stock
Estimated Time of Arrival: December 31
100 mg USD 380 In-stock
Estimated Time of Arrival: December 31
200 mg   Get quote  
500 mg   Get quote  

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Customer Review

Based on 4 publication(s) in Google Scholar

Other Forms of Pirarubicin Hydrochloride:

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Description

Pirarubicin Hydrochloride is an anthracycline antibiotics, acts as a topoisomerase II inhibitor, and is a widely used for treatment of various cancers, in particular, solid tumors.

IC50 & Target

Topoisomerase II

 

In Vitro

Pirarubicin is a topoisomerase II inhibitor[1]. Pirarubicin shows inhibitory activities against M5076 and Ehrlich cells, with IC50s of 0.366 and 0.078 μM, respectively. The cytotoxicity of Pirarubicin toward M5076 cells is lower than toward Ehrlich cells, and this is due to the much lower expression of topoisomerase II in M5076 cells than in Ehrlich cells[2]. Pirarubicin (2.5, 5, 10 μg/mL) significantly induces autophagy in a dose dependent manner in bladder cancer (T24, EJ, 5637, J82 and UM-UC-3) cells. Furthmore, Pirarubicin (5 μg/mL) induces apoptosis through inhibition of mTOR/p70S6K/4E-BP1 in bladder cancer cells, and this effect is enhanced by inhibition of autophagy[3].

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

In Vivo

Pirarubicin (18 mg/kg, i.v.) significantly elevates serum level of BNP, CK-MB, CTnT, LDH, and MDA compared with those in the control group in acute cardiac toxicity rats. Pirarubicin also lowers heart rate, and depresses R-wave voltage, and prolongation of QT intervals in the acute cardiac toxicity model[4].

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

Clinical Trial
Molecular Weight

664.10

Formula

C₃₂H₃₈ClNO₁₂

CAS No.
SMILES

O=C1C2=C(C=CC=C2OC)C(C3=C(O)C4=C([[email protected]@H](O[[email protected]@]5([H])C[[email protected]](N)[[email protected]](O[[email protected]@]6([H])OCCCC6)[[email protected]](C)O5)C[[email protected]@](C(CO)=O)(O)C4)C(O)=C31)=O.Cl

Shipping

Room temperature in continental US; may vary elsewhere.

Storage

4°C, protect from light

*In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)

Solvent & Solubility
In Vitro: 

DMSO : 20.83 mg/mL (31.37 mM; Need ultrasonic)

Preparing
Stock Solutions
Concentration Solvent Mass 1 mg 5 mg 10 mg
1 mM 1.5058 mL 7.5290 mL 15.0580 mL
5 mM 0.3012 mL 1.5058 mL 3.0116 mL
10 mM 0.1506 mL 0.7529 mL 1.5058 mL
*Please refer to the solubility information to select the appropriate solvent.
In Vivo:
  • 1.

    Add each solvent one by one:  10% DMSO    40% PEG300    5% Tween-80    45% saline

    Solubility: ≥ 2.08 mg/mL (3.13 mM); Clear solution

*All of the co-solvents are provided by MCE.
References
Cell Assay
[3]

MTS is used to analyze cell survival. Briefly, cells are plated in 96-well plates in triplicate at 2 × 103 cells per well and cultured in growth medium. Then cells are treated with pirarubicin at different concentrations (2.5 μg/mL, 5 μg/mL, 10 μg/mL) for 24 h. MTS reagent (5 mg/mL) is added and incubated at 37°C for 4 h. The absorbance is monitored at 490 nm using a microplate reader[3].

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

Animal Administration
[4]

An acute cardiac toxicity model is established by a single dose of 18 mg/kg pirarubicin through the caudal vein injection. Thirty-six rats are randomized equally to six groups: normal control, cardiac injury (THP) model, dexrazoxane (180 mg/kg), low-dose rutin (25 mg/kg), middle-dose rutin (50 mg/kg), and high-dose rutin (100 mg/kg). Rats in the rutin-treated group are administered different doses of rutin and CMC-Na for 7 days by gavage and a single dose of 18 mg/kg pirarubicin through caudal vein injection. Rats in the dexrazoxane-treated group receive sodium carboxymethylcellulose (CMC-Na) by gavage for six days. 40 mg/kg dexrazoxane is then administered to rats by intraperitoneal injection and 18 mg/kg pirarubicin is administered by caudal vein injection on day 7. Rats in the THP model group receive CMC-Na by gavage for seven days, followed by pirarubicin 18 mg/kg through the caudal vein injection on day 7. Rats in the normal control group receive CMC-Na by gavage for seven days, followed by saline through caudal vein injection on day 7[4].

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

References

Purity: 98.51%

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Keywords:

PirarubicinTHPTopoisomeraseAutophagyBacterialAntibioticInhibitorinhibitorinhibit

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Pirarubicin Hydrochloride
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