Therapeutic agent of ovarian cancer Pharmacological effects Pharmacokinetics Drug Interactions Side effects
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Olaparib

Therapeutic agent of ovarian cancer Pharmacological effects Pharmacokinetics Drug Interactions Side effects
Product Name
Olaparib
CAS No.
763113-22-0
Chemical Name
Olaparib
Synonyms
Azd2281;Olaparid;Azd-2281;4-(3-(4-(Cyclopropanecarbonyl)piperazine-1-carbonyl)-4-fluorobenzyl)phthalazin-1(2H)-one;Oraparib;Ku-0059436;Olaparib (AZD2281, Ku-0059436);CS-1931;Olapani;Olapali
CBNumber
CB02473811
Molecular Formula
C24H23FN4O3
Formula Weight
434.46
MOL File
763113-22-0.mol
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Olaparib Property

Density 
1.43
storage temp. 
-20°C
solubility 
Soluble in DMSO (up to 33 mg/ml) or in Ethanol (up to 1.7 mg/ml)
pka
12.07±0.40(Predicted)
form 
solid
color 
Off-white
Stability:
Stable for 2 years from date of purchase as supplied. Solutions in DMSO or ethanol may be stored at -20°C for up to 1 month.
InChI
InChI=1S/C24H23FN4O3/c25-20-8-5-15(14-21-17-3-1-2-4-18(17)22(30)27-26-21)13-19(20)24(32)29-11-9-28(10-12-29)23(31)16-6-7-16/h1-5,8,13,16H,6-7,9-12,14H2,(H,27,30)
InChIKey
FDLYAMZZIXQODN-UHFFFAOYSA-N
SMILES
C1(=O)C2=C(C=CC=C2)C(CC2=CC=C(F)C(C(N3CCN(C(C4CC4)=O)CC3)=O)=C2)=NN1
CAS DataBase Reference
763113-22-0
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Safety

Risk Statements 
22-38-37-36
Safety Statements 
24/25-37/39
HazardClass 
IRRITANT
HS Code 
29339900
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Hazard and Precautionary Statements (GHS)

Symbol(GHS)
Signal word
Danger
Hazard statements

H314Causes severe skin burns and eye damage

Precautionary statements

P260Do not breathe dust/fume/gas/mist/vapours/spray.

P264Wash hands thoroughly after handling.

P264Wash skin thouroughly after handling.

P280Wear protective gloves/protective clothing/eye protection/face protection.

P301+P330+P331IF SWALLOWED: Rinse mouth. Do NOT induce vomiting.

P303+P361+P353IF ON SKIN (or hair): Remove/Take off Immediately all contaminated clothing. Rinse SKIN with water/shower.

P363Wash contaminated clothing before reuse.

P405Store locked up.

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N-Bromosuccinimide Price

Cayman Chemical
Product number
10621
Product name
Olaparib
Purity
≥98%
Packaging
5mg
Price
$49
Updated
2024/03/01
Cayman Chemical
Product number
10621
Product name
Olaparib
Purity
≥98%
Packaging
10mg
Price
$68
Updated
2024/03/01
Cayman Chemical
Product number
10621
Product name
Olaparib
Purity
≥98%
Packaging
25mg
Price
$143
Updated
2024/03/01
Cayman Chemical
Product number
10621
Product name
Olaparib
Purity
≥98%
Packaging
100mg
Price
$380
Updated
2024/03/01
Usbiological
Product number
018732
Product name
Olaparib
Packaging
25mg
Price
$202
Updated
2021/12/16
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Olaparib Chemical Properties,Usage,Production

Therapeutic agent of ovarian cancer

Breast and ovarian cancer is a serious public health problem which is imposing severe threat on female. In recent years, the increasing rate of breast cancer incidence of China was even 1-2% higher than that of high-incidence countries. On the other hand, ovarian cancer still remains the most serious challenge for gynecologic oncologist because no mature approach for early stage diagnosis is available now. Upon diagnosis, about 70% cases are in advanced stage. Even subjecting to effective treatment and achieving complete alleviation, there are still 70% of patients who will get recurrence issue with 5-year survival rate hovering around 30-40%. Therefore, people are attempts to establish the three-level prevention and control measures of ovarian cancer like other chronic diseases.
There is urgent need of a new medication for ovarian cancer treatment because platinum-based chemotherapy has limited drug duration before the occurrence of intolerable side effects. Olaparib, together with other PARP inhibitors under development are all oral preparations which can be better tolerated and can have more long-term applications compared with those drugs used in conventional chemotherapy. Olaparib can prevent an enzyme which participate in cellular repair, and is suitable for patients with certain genetic mutations. The drug also has good prospects in the treatment of other cancers, opening up considerable market opportunities for olaparib.
In December 19, 2014, the FDA approved novel anti-cancer drug olaparib (Lynparza) for monotherapy to the patients of advanced ovarian cancer who has undergone at least 3 rounds of chemotherapy or patients of suspected BRCA mutations. At the same time, FDA approved the quantitation and classification of diagnostic kits for the detection of mutations in BRCA1 and BRCA2, BRACAnalysis CDx. Olaparib (Lynparza) is the first PARP inhibitor drugs which has been approved by FDA.
In February 2, 2015, the European Union Food and Drug Administration (EMA) also approved olaparib to enter into market in the 28 countries of European Union including Iceland, Liechtenstein and Norway. But the indications of EMA and FDA approved are slightly different; the former is for the BRCA gene mutation cases, and also for the maintenance therapy for patients of advanced epithelial ovarian cancer who has previously received platinum-containing chemotherapy drugs and exhibit response and subject to recurrence.

Figure 1 olaparib capsule of the anticancer drug “Lynparza” developed by the AstraZeneca Company of US.

Pharmacological effects

Olaparib is a kind of novel poly ADP-ribose polymerase (PARP) inhibitors, including PARP1, PARP2, and PARP3. PARP mediates a DNA-repair mechanism which plays a important role in DNA damage repair and apoptosis, so olaparib specifically targets on the DNA repair mechanism of the targeting cell DNA repair and take effects by attacking the critical vulnerabilities of cancer cells carrying mutations in BRCA1 and BRCA2. Owing to this mechanism, it can be used for the maintenance therapy of patients of severe recurrent ovarian cancer who has breast cancer susceptibility gene (BRCA) mutation as well as being sensitive to platinum drug.
Scientists from Harvard Medical School Dana-Farber Cancer Institute have found that the target site of olaparib is the polymerase Q (POLQ, also known POLθ). Those scientists found that a large number of patients of ovarian cancer has the genetic deficiency in the homologous recombination (homologous recombination, HR) repair pathway and dramatic up-regulated expression of POLQ greatly. Since HR is an important repair pathway for repairing broken DNA, they speculated that the major function of POLQ is to compensate for the lack of HR and participate in DNA repair.
The experiment has demonstrated that, in normal HR cells, knockout of POLQ would make HR activity increase significantly; while in HR deficient cells, the knockout of POLQ leads to cell death. POLQ contains RAD51 binding domain which can block the process of RAD51-mediated DNA repair. Related research has been published in the February 12, 2015 《Nature》journal with Raphael Ceccaldi being the first author of this research.
Studies have revealed that about 10% of ovarian cancer patients and 5% of breast cancer patients contain BRCA1 or BRCA2 mutations. Both BRCA1 and BRCA2 belong to tumor suppressor genes as the major components of HR repair pathway. Their mutation suggests the loss of function for the HR repair pathway. In the cancer model of BRCA1 or BRCA2 mutations, blocking the important component for repairing single-strand DNA breaks--PARP can kill the mutated cancer cells. Put the BRCA-deficient mice with POLQ deficient mice for hybridization will cause the death of mouse embryos shortly after birth, which means that the coexistence of two repair pathway deficiency will cause embryonic lethality.
These above findings suggest that olaparib, a kind of novel oral PARP inhibitor which is able to kill BRCA deficient cells, may be the effective drug for treating cancer patients who carry such mutations. Previously, researcher’s knowledge of the BRCA mutation hasn’t influenced patients’ choice of treatment on either ovarian cancer or breast cancer. However, after the study, which means that olaparib can be used for the targeted therapy of cancer patients who carries BRCA1 or BRCA2 gene mutations with the therapeutic target site being the genetic deficiency of cancer cell genetic defect rather than a target organ.
In ovarian and breast cancer cells, BRCA mutations are the first heavy blow to the survivability of cell because it increases their susceptibility to DNA damage. Through targeting the PARP-controlled adjuvant repair pathways, olaparib and its similar drugs achieve the second heavy blow to the survivability of cell. With the disorders of both of the two repairmen signaling pathways, the accumulation of DNA damage exert the third heavy blow to the cells.

Pharmacokinetics

Absorption
After the oral administration of olaparib through its capsule preparation, it is quickly absorbed with the plasma concentration typically reaching peak at 1-3 hour period after the administration. Multiple rounds of administration cause no significant savings (savings ratio 1.4-1.5 with 2 times per day) with achieving steady-state exposure within 3 to 4 days.
Limited information suggest that, in dose across the range of 100 to 400 mg, the increase of whole body exposure (AUC) olaparib is less than direct proportion but the PK data across the test is variable.
The co-administration of a high-fat meal causes a lower absorption rate (Tmax is delayed by 2 hours), but doesn’t significantly alter the extent of absorption of olaparib (mean AUC increased by about 20%).
Distribution
After the administration of a single dose of 400 mg olaparib, the steady-state olaparib has a mean (±SD) apparent volume of distribution of 167 ± 196 L. After the achievement of the plasma concentrations at the dose of 400mg twice daily, the in vitro protein binding rate of olaparib is approximately 82%.
Metabolism
In vitro, CYP3A4 has been shown to be primary enzymes responsible for metabolism of olaparib.
After oral administration of 14C-olaparib to female patients, unchanged olaparib accounts for the majority (70%) of the circulating radioactivity in the plasma.
It is extensively metabolized in the urine and feces with the radioactivity of drug remained unchanged accounting for 15% and 6%, respectively. The biggest part of metabolism attributes to the oxidation and the derived components which subsequently bind with glucuronide or sulfate.
Excretion
After the administration of a single dose of 400 mg olaparib, it was observed of a mean (± standard deviation) terminal plasma half-life being 11.9 ± 4.8 in hours and the apparent plasma clearance being 8.6 ± 7.1L/h.
After a single dose of 14C-olaparib, during the seven days of collection, 86% of the administered radioactivity was recovered with 44% going through urine and 42% going through feces. Most of the material is excreted as metabolites.
According to the preliminary data of special efforts from renal impairment test, when olaparib is administrated by patients of mild renal impairment (CLcr = 50-80 mL/min; N = 14) and compared to patients with normal renal function (CLcr> 80 mL/min; N = 8), the mean AUC and Cmax of olaparib were increased by 1.5 and 1.2 times, respectively. There are no data available for the patients with CLcr <50 mL/min or patients subjecting to dialysis.

Drug Interactions

In vitro, olaparib is a inhibitor of the CYP3S4 but the inducing agent of CYP2B6 upon the higher concentration achieved clinically. Olaparib has small or no inhibitory effects on other CYP isozymes. In vitro studies have ever shown that olaparib is the substrate of CYP3A4.
According from a set of Drug-interaction test data (N = 57), when olaparib is administrated with itraconazole, a potent CYP3A inhibitor, in combination, the AUC and Cmax of olaparib were increased by 2.7-and 1.4-fold, respectively. The stimulation based on the physiologically pharmacokinetic (PBPK) model suggests a moderate inhibitor of CYP3A (fluconazole) can increase the AUC and Cmax of olaparib, respectively, by 2-and 1.1-fold.
According a set of Drug-interaction test data (N = 22), when olaparib is administrated with rifampicin, a potent CYP3A inducer, in combination, the AUC and Cmax of olaparib were reduced by 87% and 71 %, respectively. Stimulation based on PBPK model suggests one kind of moderate CYP3A inducers (efavirenz) may reduce the AUC and Cmax of olaparib by 50-60% and 20-30%, respectively.
In vitro studies have ever shown that olaparib is the substrate of P-gp and the inhibitors of BCRP, OATP1B1, OCT1, OCT2, OAT3, MATE1 and MATE2K. It is still not clear about the clinical relevance of these findings.
The above information is edited by the Chemicalbook of Dai Xiongfeng.

Side effects

1. The most common adverse reaction in clinical trials≥20%) include anemia, nausea, fatigue (including lack in strength), vomiting, diarrhea, taste disturbance, indigestion, headache, loss of appetite, nasopharyngitis/pharyngitis/URI, cough, arthralgia/musculoskeletal pain, myalgia, back pain, dermatitis/rash and abdominal pain/discomfort.
2. The most common laboratory abnormalities (≥25%) is increased creatinine, increased red blood cell mean volume, reduced hemoglobin, reduced lymphocytes, reduced absolute neutrophil count, and thrombocytopenia.

Description

Olaparib, marketed by AstraZeneca under the brand name Lynparza , was approved in the USA in December 2014 as a targeted, single-agent therapy for the treatment of germline BRCA-mediated advanced ovarian cancer.Olaparib, originally developed by KuDOS pharmaceuticals and later by AstraZeneca, functions as a poly ADP ribose polymerase inhibitor and has been specifically approved for patients who have received three or more treatments of chemotherapy. In clinical trials, the drug prolonged progression- free survival for patients suffering from platinum-sensitive recurrent serous ovarian cancer. Olaparib is also currently in various phases of investigation for treatment of breast, gastric, prostate, pancreatic and non-small cell lung cancer.

Chemical Properties

White Solid

Uses

Olaparib is a potent poly(ADP-ribose) polymerase (PARP) inhibitor. Olaparib has been shown to induce significant killing of ATM-deficient lymphoid tumor cells in vitro and in vivo. Recent studies show that Olaparib increases radiosensitivity of a lung tumor xenograft, making it a potential candidate for use in combination with radiotherapy.

Definition

ChEBI: Olaparib is a member of the class of N-acylpiperazines obtained by formal condensation of the carboxy group of 2-fluoro-5-[(4-oxo-3,4-dihydrophthalazin-1-yl)methyl]benzoic acid with the free amino group of N-(cyclpropylcarbonyl)piperazine; used to treat advanced ovarian cancer. It has a role as an antineoplastic agent, an EC 2.4.2.30 (NAD(+) ADP-ribosyltransferase) inhibitor and an apoptosis inducer. It is a N-acylpiperazine, a member of cyclopropanes, a member of monofluorobenzenes and a member of phthalazines.

Biological Activity

Many of the products generated by alkylating agents on DNA can be efficiently repaired by normal base excision repair (BER). Some poly(ADP-ribose) polymerases (PARPs) assist in the repair of single-strand DNA nicks, an important step in BER. Olaparib is a potent inhibitor of PARP1 and PARP2 (IC50 = 5 and 1 nM, respectively) but is less effective against the PARP tankyrase-1 (IC50 = 1.5 μM). It can be used in cells and in animals, alone or in combination therapy with alkylating agents, to block BER and increase cancer cell death.[Cayman Chemical]

Clinical Use

Human poly (ADP-ribose) polymerase enzymes inhibitor:
Treatment of platinum-sensitive relapsed BRCAmutated high grade serous epithelial ovarian, fallopian tube, or primary peritoneal cancer

Synthesis

This optimized synthesis begins with reaction of commercially available dimethyl phosphite and 2-carboxybenzaldehyde (201) to generate the corresponding phosphonate ester in 95% yield and 95% purity after aqueous workup.190 Addition of aldehyde 202 to this phosphonate ester intermediate in the presence of triethylamine led to formation of olefins 203a/203b in 96% yield as a 1:1 mixture of E/Z isomers. From olefins 203a/203b, a one-pot, three-step sequence was next performed to provide access to dihydrophthalazinyl acid 204. First, lactone ring-opening and nitrile hydrolysis was facilitated by reaction with aqueous sodium hydroxide under elevated temperatures, allowing for subsequent in situ formation of the corresponding dihydrophthalazine intermediate after addition of hydrazine hydrate. Acidification and precipitation of product with 2 N HCl led to isolation of the desired material in 77% yield and 96% purity after filtration. Further coupling of carboxylic acid 204 with Bocpiperazine (205) (HBTU, DIPEA, DMA) and subsequent removal of the carbamate with HCl/EtOH provided intermediate 206 in 46% yield from 204, relying on a pH-controlled workup procedure to enable isolation of material in high purity (94%) without requiring chromatography. The final step of the olaparib synthesis was completed via treatment of piperazine 206 with cyclopropane carbonyl chloride (207) and triethylamine, leading to isolation of olaparib in 90% yield and 99.3% purity after distillation.

Drug interactions

Potentially hazardous interactions with other drugs
Antibacterials: concentration possibly increased by ciprofloxacin, clarithromycin and erythromycin - avoid or reduce olaparib dose to 150 mg twice daily; avoid with rifabutin and rifampicin.
Antidepressants: avoid with St John’s wort.
Antiepileptics: avoid with carbamazepine, phenobarbital and phenytoin.
Antifungals: concentration increased by itraconazole and possibly fluconazole - avoid or reduce olaparib dose to 150 mg twice daily.
Antipsychotics: avoid with clozapine - increased risk of agranulocytosis.
Antivirals: concentration possibly increased by boceprevir, ritonavir and telaprevir - avoid or reduce olaparib dose to 150 mg twice daily; avoid with nevirapine.
Calcium channel blockers: concentration possibly increased by diltiazem and verapamil - avoid or reduce olaparib dose to 150 mg twice daily.
Cobicistat: concentration possibly increased - avoid or reduce olaparib dose to 150 mg twice daily.
Grapefruit juice: avoid concomitant use.
Oestrogens and progestogens: possibly reduced contraceptive effect.

Metabolism

In vitro, CYP3A4 was shown to be the main enzyme responsible for the metabolism of olaparib. The majority of the metabolism was due to oxidation reactions with a number of the components produced undergoing subsequent glucuronide or sulfate conjugation.
Following a single dose of [14C]-olaparib, approximately 86% of the dose was recovered within a 7-day collection period, approximately 44% via the urine and 42% via the faeces. The majority of olaparib was excreted as metabolites.

storage

Store at -20°C

Mode of action

Olaparib is a small molecule inhibitor of the nuclear enzyme poly(ADP-ribose) polymerase (PARP) with potential chemosensitizing, radiosensitizing, and antineoplastic activities. Olaparib selectively binds to and inhibits PARP, inhibiting PARP-mediated repair of single strand DNA breaks; PARP inhibition may enhance the cytotoxicity of DNA-damaging agents and may reverse tumor cell chemoresistance and radioresistance. PARP catalyzes post-translational ADP-ribosylation of nuclear proteins and can be activated by single-stranded DNA breaks.

References

1) Menear?et al. (2008),?4-[3-(4-Cyclopropanecarbonylpiperazine-1-carbonyl)-4-fluorobenzyl]-2H-phthalazin-1-one: a novel bioavailable inhibitor of poly(ADP-ribose)polymerase-1;? J. Med. Chem.,?51?6581
2) Rottenberg?et al. (2008),?High sensitivity of BRCA1-deficient mammary tumors to the PARP inhibitor AZD2281 alone and in combination with platinum drugs; Proc. Natl. Acad. Sci. USA,?105?17079
3) Avila-Arroyo?et al. (2015),?Synergistic effect of Trabectedin and Olaparib combination regimen in breast cancer cell lines; J. Breast Cancer,?18?329
4) Xu?et al. (2015),?Combined olaparib and oxaliplatin inhibits tumor proliferation and induces G2/M arrest and γ-H2AX foci formation in colorectal cancer; Onco. Targets Ther.,?8?3047
5) Ghonim?et al. (2015),?PARP is activated in human asthma and its inhibition by olaparib blocks house dust mite-induced disease in mice; Clin. Sci.(Lond),?129?951

Olaparib Preparation Products And Raw materials

Raw materials

Preparation Products

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Olaparib Suppliers

Shanghai Jinyin Biological Technology Co., Ltd
Tel
021-20986266 18019349802
Email
814527417@qq.com
Country
China
ProdList
461
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58
ChemFuture PharmaTech (Jiangsu) Ltd
Tel
5108538618
Fax
86 510 85386988-8017
Email
suger.wang@chemfuture.com
Country
China
ProdList
822
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65
Beijing Mesochem Technology Co., Ltd.
Tel
010-57862036 18811083386
Email
msales@mesochem.com
Country
China
ProdList
188
Advantage
58
Wuhan Wiseman Bioengineering Co.,Ltd
Tel
027-59506022 13419526507
Fax
027-59506022
Email
13419526507@163.com
Country
China
ProdList
2945
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58
AnHui HaiKang Pharmaceutical Co., Ltd.
Tel
0556-5800026 17709662922
Email
melrose@worldpharma.cn
Country
China
ProdList
212
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55
Shanghai Biobond Pharmaceutical Co.,Ltd.
Tel
21-68719686 18917373795
Fax
021-68719686
Email
sales@sh-biobond.cn
Country
China
ProdList
78
Advantage
58
Cangzhou Kangrui Medical Technology Co., LTD
Tel
18632776803
Email
355803330@qq.com
Country
China
ProdList
523
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58
Zhejiang Brunova Technology Co., Ltd.
Tel
17857108485
Email
info@zjbrunova.com
Country
China
ProdList
51
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58
TIANJIN PHARMACN MEDICAL TECHNOLOGY CO.,LTD.
Tel
022-60182192,1339732154 18722583064
Fax
86-22-60979672
Email
marketing@pharmacn.com
Country
China
ProdList
112
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61
Shanghai Boyle Chemical Co., Ltd.
Tel
Fax
86-21-57758967
Email
sales@boylechem.com
Country
China
ProdList
2923
Advantage
55
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View Lastest Price from Olaparib manufacturers

Dorne Chemical Technology co. LTD
Product
Olaparib 763113-22-0
Price
US $1.00/g
Min. Order
1g
Purity
99%
Supply Ability
100kg
Release date
2024-03-26
Shandong Hanjiang Chemical Co., Ltd
Product
Olaparib 763113-22-0
Price
US $0.00/kg
Min. Order
1kg
Purity
0.99
Supply Ability
10T
Release date
2024-01-19
Zibo Wei Bin Import & Export Trade Co. Ltd.
Product
Olaparib 763113-22-0
Price
US $100.00/kg
Min. Order
1kg
Purity
99%
Supply Ability
1t
Release date
2023-07-11

763113-22-0, OlaparibRelated Search:


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