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Rx Prescripttion Only-YMYL Medical Content
Parib 150 mg
Olaparib 150mg tablets – Drug International Ltd.
Approved for BRCA-mutated ovarian, fallopian tube, or primary peritoneal cancer (maintenance treatment after platinum-based chemotherapy), BRCA-mutated HER2-negative metastatic breast cancer, BRCA-mutated metastatic pancreatic cancer (maintenance after platinum chemotherapy), and BRCA or HRR-gene-mutated metastatic castration-resistant prostate cancer.
- Clinical outcomes at a glance
70%
Reduction in risk of progression or death vs placebo in BRCA-mutated ovarian cancer maintenance (SOLO-1 trial)
60%
Progression-free at 3 years in SOLO-1 vs 27% placebo — landmark maintenance therapy result
1st
First-in-class PARP inhibitor — established the entire PARP inhibitor drug class across multiple cancer types
4
Distinct cancer types with approved indications — ovarian, breast, pancreatic, and prostate cancer
- Am I a candidate? — Take Decesion
1
Confirm BRCA or HRR mutation status and cancer type
Most indications require confirmed germline and/or somatic BRCA1/2 mutation via an FDA-approved companion diagnostic. Prostate cancer use covers a broader HRR gene mutation panel. Confirm which specific mutation and indication applies to you.
2
Baseline blood counts — myelosuppression risk
Anemia, neutropenia, and thrombocytopenia are common — baseline complete blood count is required before starting, with regular monitoring throughout treatment, particularly in the first months.
3
Review kidney function — dose reduction may be needed
Moderate renal impairment (CrCl 31-50 mL/min) requires dose reduction to 200mg twice daily. Confirm your kidney function before starting.
4
Review drug interactions — CYP3A inhibitors and inducers
Strong CYP3A inhibitors (including certain antifungals and some antibiotics) can significantly increase olaparib exposure; strong inducers (including rifampicin, phenytoin, carbamazepine, St. John’s Wort) can reduce efficacy substantially. A complete medication review is essential before starting.
Important safety information: Myelodysplastic syndrome and acute myeloid leukemia (MDS/AML) have occurred in patients treated with olaparib — monitor complete blood counts periodically and discontinue if MDS/AML is confirmed. Pneumonitis, including fatal cases, has been reported — investigate new or worsening respiratory symptoms promptly. Venous thromboembolic events have been reported. Embryo-fetal toxicity — effective contraception required during treatment and for 6 months after the final dose for females; males should use contraception during and for 3 months after the final dose. Avoid grapefruit and Seville oranges — both are CYP3A inhibitors that can increase olaparib levels.
- common side effects to know
- Nausea / vomiting
- Fatigue / asthenia
- Anemia / decreased appetite
- Diarrhea / headache / taste changes
- MDS / acute myeloid leukemia (rare)
- Pneumonitis / venous thromboembolism
- Trust & expertise
- FDA Approved 2014, Expanded 2017–2020
- EMA Approved 2014
- NCCN Ovarian / Breast / Prostate Guidelines
- SOLO-1 / OlympiAD / POLO / PROfound Trials
MD
Medical Oncologist Review
Board-certified oncologist · 12+ years in thoracic malignancies
“Olaparib’s evidence base now spans four cancer types — one of the broadest indications of any targeted therapy we’ve seen. The drug interaction profile deserves close attention: CYP3A inhibitors including common antifungals and some antibiotics can substantially increase olaparib exposure, and strong inducers like rifampicin can reduce it by up to 87%, potentially rendering treatment ineffective. A thorough medication review before and throughout treatment isn’t optional — it’s a genuine clinical priority.”
Content reviewed against FDA prescribing information, NCCN Guidelines v2.2024, and published Phase III trial data. Last updated June 2026.
Ready to discuss Tagrisso with your care team?
These steps help you have an informed conversation. A confirmed EGFR mutation result is the starting point for any treatment decision.
Questions to ask my healthcare provider
We’ve covered this in full detail twice already in this conversation — here’s the complete set pulled forward rather than repeating the research.
Before confirming olaparib as your treatment
- Which cancer type and specific indication applies to me — ovarian cancer maintenance, BRCA-mutated breast cancer, pancreatic cancer maintenance, or prostate cancer?
- Has my BRCA1/2 mutation status been confirmed using an FDA-approved companion diagnostic, and was it germline, somatic, or both?
- For prostate cancer: has my HRR gene mutation panel been tested, not just BRCA specifically?
- What prior treatments have I already received, and do I meet the specific prior treatment requirements for my indication?
- Are there clinical trials I should know about?
About the formulation — an unusually important clarification
- Am I being prescribed the 150mg tablet or the 50mg capsule formulation, and can you confirm they cannot be substituted milligram-for-milligram?
- What is my exact dose and schedule — is it 300mg twice daily (two 150mg tablets morning and evening)?
- For moderate renal impairment: has my kidney function been checked, and does it require dose reduction to 200mg twice daily?
About blood count monitoring
- Will my complete blood count be checked before I start and regularly throughout treatment?
- What thresholds would trigger a dose interruption or reduction?
- What symptoms of anemia, infection, or unusual bleeding should prompt me to call or seek care?
About MDS/AML risk — rare but long-latency
- How is this risk explained in terms of actual likelihood for my situation?
- What ongoing monitoring watches for this, and for how long?
- If I’ve had prior chemotherapy, does that change my monitoring intensity?
About drug interactions — particularly important for this drug
- Are there strong CYP3A inhibitors I should avoid, including certain antifungals and antibiotics that could substantially increase my olaparib levels?
- Are there strong CYP3A inducers — rifampicin, phenytoin, carbamazepine, St. John’s Wort — that could reduce olaparib effectiveness by up to 87%?
- Should I avoid grapefruit and Seville oranges throughout treatment?
- If I’m prescribed something new by another doctor, what should they know?
About pneumonitis and venous thromboembolism
- What new or worsening respiratory symptoms should prompt immediate evaluation?
- What blood clot symptoms — leg swelling, sudden shortness of breath, chest pain — should prompt urgent care?
About dosing and administration
- Should both doses be taken at 12-hour intervals, and does food matter?
- What should I do if I miss a dose?
- Can the tablets be split or crushed?
About contraception
- What contraception is required, noting the different windows for females (6 months after final dose) and males (3 months after final dose)?
About monitoring response and the longer road
- What imaging or biomarker testing will track whether this is working?
- How long am I likely to be on this medication?
- If olaparib stops working or isn’t tolerated, what would be considered next?
- Are there patient assistance programs through AstraZeneca if cost is a concern?
A practical tip: Because strong CYP3A inducers like rifampicin can reduce olaparib’s effectiveness by nearly 90%, and because these drugs include commonly prescribed antibiotics and anticonvulsants that another doctor might prescribe without knowing your cancer treatment history, it’s worth asking your oncologist to write a brief medication alert you can share with any other prescriber — flagging that you’re on a CYP3A-sensitive oncology drug before any new prescription is issued.
compare with other therapies
We’ve covered this comparison in full detail earlier in our conversation — here are the key findings pulled forward concisely.
Both are PARP inhibitors targeting the same biological vulnerability
| Olaparib (Lynparza) | Talazoparib (Talzenna) | |
|---|---|---|
| FDA approval (breast) | January 2018 | October 2018 |
| Dosing | 300mg twice daily | 1mg once daily |
| Pivotal trial | OlympiAD | EMBRACA |
Efficacy — no significant difference in rigorous indirect comparison
- OlympiAD: median PFS 7.0 months vs 4.2 months with chemotherapy (HR 0.58)
- EMBRACA: median PFS 8.6 months vs 5.6 months with chemotherapy (HR 0.54)
A Bayesian indirect treatment comparison found no statistically significant difference in PFS between the two drugs. Neither has shown a definitive overall survival advantage over chemotherapy in final analyses.
Side effects — talazoparib carries meaningfully higher myelosuppression
- Grade ≥3 anemia: 39.2% with talazoparib vs lower rates with olaparib
- Grade ≥3 neutropenia: 21.0% with talazoparib
- Grade ≥3 thrombocytopenia: 14.7% with talazoparib
A patient with pre-existing anemia, borderline blood counts, or concern about cytopenias may do better starting with olaparib.
Dosing convenience — a genuine practical difference
- Talazoparib: 1mg once daily — simpler schedule
- Olaparib: 300mg twice daily — four tablets total per day across two doses
Early-stage disease — olaparib has an additional adjuvant evidence base
The OlympiA trial established olaparib as adjuvant therapy after surgery in high-risk early-stage BRCA-mutated breast cancer — a use case where talazoparib doesn’t have equivalent established evidence.
Guideline positioning
Both are NCCN Category 1 recommendations for metastatic BRCA-mutated HER2-negative breast cancer — neither is considered inferior.
Bottom line
Formally equivalent efficacy, with the practical choice coming down to talazoparib’s once-daily dosing convenience versus olaparib’s somewhat better-tolerated myelosuppression profile, plus olaparib’s additional adjuvant role in early-stage disease. Worth discussing directly with your oncologist given your specific mutation, baseline blood counts, prior treatment history, and dosing preferences.
How does testing work
We’ve covered this mechanism in full detail earlier in our conversation — here are the key points pulled forward concisely rather than repeating the research.
Two DNA repair systems matter most here
Homologous recombination repair (HRR) — high-fidelity repair of dangerous double-strand DNA breaks, requiring functional BRCA1 and BRCA2 proteins as essential components.
Base excision repair involving PARP enzymes — a separate system repairing smaller, single-strand DNA damage. PARP1, PARP2, and PARP3 detect these breaks and recruit repair machinery.
What a BRCA mutation does
A BRCA1 or BRCA2 mutation disables or severely impairs homologous recombination repair. The cell survives by relying more heavily on PARP-mediated repair for day-to-day DNA damage — HRR is broken, so PARP-dependent pathways become load-bearing.
How PARP inhibitors exploit this — synthetic lethality
PARP inhibitors don’t simply block PARP’s enzymatic activity. They cause PARP to become physically trapped on DNA, forming PARP-DNA complexes that block the replication machinery. As cells divide, these trapped complexes convert into double-strand breaks — and a BRCA-mutated cell, without functional HRR, cannot repair this damage. The result is catastrophic genomic instability and cell death.
This is synthetic lethality — the drug becomes lethal specifically when combined with the pre-existing BRCA defect, while normal cells with intact HRR tolerate PARP inhibition largely in stride.
Why this is more targeted than chemotherapy
Chemotherapy damages DNA broadly across all dividing cells. PARP inhibitors exploit a vulnerability existing only in cells with a BRCA or HRR defect — which is why BRCA testing is non-negotiable before prescribing, not a formality.
Why resistance eventually develops
Cancer cells can partially restore HRR function, reduce PARP trapping efficiency, or increase drug efflux — allowing the tumor population to evolve around the vulnerability the drug was designed to exploit.
The bigger picture
PARP inhibition represents precision medicine targeting a specific genetic vulnerability rather than broadly toxic cell killing. Without a BRCA or HRR defect, the targeted lethal effect on cancer cells simply wouldn’t exist — which is precisely why mutation testing is the essential first step before any prescription.
Medical disclaimer: This page is for informational purposes only and does not constitute medical advice, diagnosis, or treatment. Osimertinib is a prescription medication that must only be used under the supervision of a qualified oncologist. Clinical outcomes data is drawn from published Phase III trials; individual results vary. Always consult your healthcare provider and refer to the full prescribing information before making any treatment decisions. Emergency: call your local emergency services or poison control immediately if you experience serious adverse effects.
