Pirarubicin

Topo II inhibitor;antineoplastic;analogue of doxorubicin CAS# 72496-41-4

Pirarubicin

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Quality Control of Pirarubicin

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Chemical structure

Pirarubicin

3D structure

Chemical Properties of Pirarubicin

Cas No. 72496-41-4 SDF Download SDF
PubChem ID 3033521 Appearance Powder
Formula C32H37NO12 M.Wt 627.64
Type of Compound N/A Storage Desiccate at -20°C
Synonyms THP
Solubility DMSO : 50 mg/mL (79.66 mM; Need ultrasonic)
Chemical Name (9S)-7-[(2R,4S,5S,6S)-4-amino-6-methyl-5-[(2R)-oxan-2-yl]oxyoxan-2-yl]oxy-6,9,11-trihydroxy-9-(2-hydroxyacetyl)-4-methoxy-8,10-dihydro-7H-tetracene-5,12-dione
SMILES CC1C(C(CC(O1)OC2CC(CC3=C(C4=C(C(=C23)O)C(=O)C5=C(C4=O)C=CC=C5OC)O)(C(=O)CO)O)N)OC6CCCCO6
Standard InChIKey KMSKQZKKOZQFFG-YHKVCKOMSA-N
Standard InChI InChI=1S/C32H37NO12/c1-14-31(45-21-8-3-4-9-42-21)17(33)10-22(43-14)44-19-12-32(40,20(35)13-34)11-16-24(19)30(39)26-25(28(16)37)27(36)15-6-5-7-18(41-2)23(15)29(26)38/h5-7,14,17,19,21-22,31,34,37,39-40H,3-4,8-13,33H2,1-2H3/t14-,17-,19?,21+,22-,31+,32-/m0/s1
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Biological Activity of Pirarubicin

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

References:
[1]. Takigawa N, et al. Cytotoxic effect of topoisomerase II inhibitors against adriamycin- and etoposide-resistant small cell lung cancer sublines. Gan To Kagaku Ryoho. 1993 May;20(7):929-35. [2]. Nagai K, et al. Relationships between the in vitro cytotoxicity and transport characteristics of pirarubicin and doxorubicin in M5076 ovarian sarcoma cells, and comparison with those in Ehrlich ascites carcinoma cells. Cancer Chemother Pharmacol. 2002 Mar;49(3):244-50. Epub 2002 Jan 8. [3]. Li K, et al. Pirarubicin induces an autophagic cytoprotective response through suppression of the mammalian target of rapamycin signaling pathway in human bladder cancer cells. Biochem Biophys Res Commun. 2015 May 1;460(2):380-5. [4]. Wang YD, et al. Cardioprotective effects of rutin in rats exposed to pirarubicin toxicity. J Asian Nat Prod Res. 2017 Oct 27:1-13.

Protocol

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].

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].

References:
[1]. Takigawa N, et al. Cytotoxic effect of topoisomerase II inhibitors against adriamycin- and etoposide-resistant small cell lung cancer sublines. Gan To Kagaku Ryoho. 1993 May;20(7):929-35. [2]. Nagai K, et al. Relationships between the in vitro cytotoxicity and transport characteristics of pirarubicin and doxorubicin in M5076 ovarian sarcoma cells, and comparison with those in Ehrlich ascites carcinoma cells. Cancer Chemother Pharmacol. 2002 Mar;49(3):244-50. Epub 2002 Jan 8. [3]. Li K, et al. Pirarubicin induces an autophagic cytoprotective response through suppression of the mammalian target of rapamycin signaling pathway in human bladder cancer cells. Biochem Biophys Res Commun. 2015 May 1;460(2):380-5. [4]. Wang YD, et al. Cardioprotective effects of rutin in rats exposed to pirarubicin toxicity. J Asian Nat Prod Res. 2017 Oct 27:1-13.

Pirarubicin Dilution Calculator

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Pirarubicin Molarity Calculator

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Preparing Stock Solutions of Pirarubicin

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 1.5933 mL 7.9664 mL 15.9327 mL 31.8654 mL 39.8318 mL
5 mM 0.3187 mL 1.5933 mL 3.1865 mL 6.3731 mL 7.9664 mL
10 mM 0.1593 mL 0.7966 mL 1.5933 mL 3.1865 mL 3.9832 mL
50 mM 0.0319 mL 0.1593 mL 0.3187 mL 0.6373 mL 0.7966 mL
100 mM 0.0159 mL 0.0797 mL 0.1593 mL 0.3187 mL 0.3983 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

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Background on Pirarubicin

Pirarubicin is an analogue of the anthracycline anti-neoplastic doxorubicin. Intercalates into DNA and interacts with Topo II (topoisomerase II) and supressing DNA replication. Pirarubicin is an inhibitor of Topo II.

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References on Pirarubicin

Pronounced Cellular Uptake of Pirarubicin versus That of Other Anthracyclines: Comparison of HPMA Copolymer Conjugates of Pirarubicin and Doxorubicin.[Pubmed:27934482]

Mol Pharm. 2016 Dec 5;13(12):4106-4115.

Many conjugates of water-soluble polymers with biologically active molecules were developed during the last two decades. Although, therapeutic effects of these conjugates are affected by the properties of carriers, the properties of the attached drugs appear more important than the same carrier polymer in this case. Pirarubicin (THP), a tetrahydropyranyl derivative of doxorubicin (DOX), demonstrated more rapid cellular internalization and potent cytotoxicity than DOX. Here, we conjugated the THP or DOX to N-(2-hydroxypropyl)methacrylamide copolymer via a hydrazone bond. The polymeric prodrug conjugates, P-THP and P-DOX, respectively, had comparable hydrodynamic sizes and drug loading. Compared with P-DOX, P-THP showed approximately 10 times greater cellular uptake during a 240 min incubation and a cytotoxicity that was more than 10 times higher during a 72-h incubation. A marginal difference was seen in P-THP and P-DOX accumulation in the liver and kidney at 6 h after drug administration, but no significant difference occurred in the tumor drug concentration during 6-24 h after drug administration. Antitumor activity against xenograft human pancreatic tumor (SUIT2) in mice was greater for P-THP than for P-DOX. To sum up, the present study compared the biological behavior of two different drugs, each attached to an N-(2-hydroxypropyl)methacrylamide copolymer carrier, with regard to their uptake by tumor cells, body distribution, accumulation in tumors, cytotoxicity, and antitumor activity in vitro and in vivo. No differences in the tumor cell uptake of the polymer-drug conjugates, P-THP and P-DOX, were observed. In contrast, the intracellular uptake of free THP liberated from the P-THP was 25-30 times higher than that of DOX liberated from P-DOX. This finding indicates that proper selection of the carrier, and especially conjugated active pharmaceutical ingredient (API) are most critical for anticancer activity of the polymer-drug conjugates. THP, in this respect, was found to be a more preferable API for polymer conjugation than DOX. Hence the treatment based on enhanced permeability and retention (EPR) effect that targets more selectively to solid tumors can be best achieved with THP, although both polymer conjugates of DOX and THP exhibited the EPR effects and drug release profiles in acidic pH similarly.

Inducing Optimal Antitumor Immune Response through Coadministering iRGD with Pirarubicin Loaded Nanostructured Lipid Carriers for Breast Cancer Therapy.[Pubmed:27936775]

Mol Pharm. 2017 Jan 3;14(1):296-309.

Chemotherapeutic agents trigger antitumor immune response through inducing immunogenic tumor cell death. However, severe toxicity to immune system and insufficient immunogenic cell death hinder chemotherapy from arousing efficient antitumor immunity in vivo. In this study, the cytotoxic drug, Pirarubicin (THP), was entrapped into nanostructured lipid carriers (NLC); THP-NLC significantly reduced the toxicity of THP to immune system and improved immune status of breast cancer bearing mice. When THP-NLC was coinjected with iRGD (a tumor-penetrating peptide), drug accumulation in tumors was greatly elevated, which led to significant control of tumor growth and increase of immunogenic tumor cell death. Subsequently, the cytotoxic T lymphocytes (CD3(+) and CD8(+) cells) infiltration and cytokine (IFN-gamma and INF-alpha) secretion in tumors were heavily increased. The efficient T-cell dependent control of tumors in the late stage and the lower side effects contributed to the longest whole survival of THP-NLC + iRGD treated mice. Therefore, the coadministration of THP-NLC with iRGD resulted in increased tumor cell direct-killing death and enhanced antitumor immune response. Our results illustrated that THP could serve as an immunogenic cell death inducer and the proposed drug delivery strategy might impact cancer immunotherapy by arousing increased immunogenic tumor cell death.

Rutin Protects against Pirarubicin-Induced Cardiotoxicity through TGF-beta1-p38 MAPK Signaling Pathway.[Pubmed:28367221]

Evid Based Complement Alternat Med. 2017;2017:1759385.

We investigated the potential protective effect of rutinum (RUT) against Pirarubicin- (THP-) induced cardiotoxicity. THP was used to induce toxicity in rat H9c2 cardiomyoblasts. Positive control cells were pretreated with a cardioprotective agent dexrazoxane (DZR) prior to treatment with THP. Some of the cells were preincubated with RUT and a p38 mitogen-activated protein kinase (MAPK) inhibitor, SB203580, both individually and in combination, prior to THP exposure. At a dose range of 30-70 muM, RUT significantly prevented THP-induced reduction in cell viability; the best cardioprotective effect was observed at a dose of 50 muM. Administration of RUT and SB203580, both individually as well as in combination, suppressed the elevation of intracellular ROS, inhibited cell apoptosis, and reversed the THP-induced upregulation of TGF-beta1, p-p38 MAPK, cleaved Caspase-9, Caspase-7, and Caspase-3. A synergistic effect was observed on coadministration of RUT and SB203580. RUT protected against THP-induced cardiotoxicity by inhibition of ROS generation and suppression of cell apoptosis. The cardioprotective effect of RUT appears to be associated with the modulation of the TGF-beta1-p38 MAPK signaling pathway.

Acute and late toxicities of pirarubicin in the treatment of childhood acute lymphoblastic leukemia: results from a clinical trial by the Japan Association of Childhood Leukemia Study.[Pubmed:27858183]

Int J Clin Oncol. 2017 Apr;22(2):387-396.

BACKGROUND: Anthracyclines are used to treat childhood acute lymphoblastic leukemia (ALL). Even when administered at low doses, these agents are reported to cause progressive cardiac dysfunction. We conducted a clinical trial comparing the toxicities of two anthracyclines, Pirarubicin (THP) and daunorubicin (DNR), in the treatment of childhood ALL. The results from our study that relate to acute and late toxicities are reported here. METHODS: 276 children with B-ALL were enrolled in the trial from April 1997 to March 2002 and were randomly assigned to receive a regimen including either THP (25 mg/m(2) x 11) or DNR (30 mg/m(2) x 11). Acute toxicity was prospectively assessed based on the National Cancer Institute Common Toxicity Criteria. Acute hematological toxicity was also examined via some parameters. Patients with event-free survival of >5 years were retrospectively surveyed for cardiac function at 5 and 10 years and at the most recent assessment more than 10 years from the onset of ALL. RESULTS: Acute hematological toxicity in the early phase was more significant in the THP arm. Based on ultrasound cardiography, cardiac function was impaired in both groups during the follow-up period, but there was no significant difference between the groups except for a greater decline in fractional shortening on ultrasound cardiography in the DNR arm. CONCLUSIONS: While acute hematological toxicity was more significant in the THP arm, THP also appeared to be less cardiotoxic. However, the evaluation of late cardiotoxicity was limited because only a few subjects were followed beyond 10 years after ALL onset. Considering that the THP regimen produced an EFS rate comparable with that of the DNR regimen, the efficacy and toxicity of THP at reduced doses should be studied in order to identify potentially safer regimens.

Description

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

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