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Rx Prescripttion Only-YMYL Medical Content
Olarigen 150 mg
Olaparib 150mg tablets – General Medicinals 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 survival at 3 years in SOLO-1 (olaparib) vs 27% placebo — a 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 this specific tablet formulation.
4
Confirm you have been prescribed the tablet, not the capsule formulation
Olaparib 150mg tablets and 50mg capsules cannot be substituted milligram-for-milligram — confirm with your pharmacist each time you refill that you are receiving the same formulation as previously dispensed.
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.
- 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 was the first PARP inhibitor to reach patients and has since demonstrated meaningful benefit across four distinct cancer types — a breadth of evidence that remains remarkable. The formulation distinction deserves special attention at every prescription and refill: the 150mg tablet and the 50mg capsule are not interchangeable milligram-for-milligram, and getting this wrong is a genuinely impactful dispensing error that patients should be empowered to catch themselves.”
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 covered this in full detail just a few pages back for the Olanib page — 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 for each other on a milligram-to-milligram basis?
- 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 a reduced dose of 200mg twice daily?
About blood count monitoring
- Will my complete blood count be checked before I start and regularly throughout treatment?
- What blood count thresholds would trigger a dose interruption or reduction?
- What symptoms of anemia — unusual fatigue, dizziness, shortness of breath — or infection 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 blood count monitoring watches for this, and for how long?
- If I’ve had prior chemotherapy, does that change my monitoring intensity?
- What symptoms outside of scheduled blood tests should prompt me to flag something?
About kidney function
- What is my current creatinine clearance, and does it affect my starting dose?
- Will my kidney function be monitored during treatment?
About pneumonitis risk
- What new or worsening respiratory symptoms should prompt immediate evaluation?
- How will drug-related lung changes be distinguished from my underlying cancer’s effects?
About venous thromboembolism risk
- Do I have personal risk factors for blood clots that are particularly relevant here?
- What symptoms — leg swelling or pain, sudden shortness of breath, chest pain — should prompt urgent care?
About dosing and administration
- Should both doses be taken at roughly 12-hour intervals, and does food matter?
- What should I do if I miss a dose?
- Can the tablets be split or crushed, or must they be swallowed whole?
About drug interactions
- Are there strong CYP3A inhibitors or inducers I should avoid — I understand these can significantly affect olaparib’s blood levels?
- If I’m prescribed something new by another doctor, what should they know?
About contraception
- What contraception is required during treatment — and for how long after the final dose, noting the different windows for females (6 months) and males (3 months)?
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 olaparib exists in two formulations — 150mg tablets and 50mg capsules — that cannot be substituted milligram-for-milligram, confirm explicitly with your pharmacist at every refill which formulation you’ve been dispensed. This is one of the few drugs in oncology where a seemingly minor dispensing variation could result in meaningfully incorrect dosing, and being aware of this as a patient puts you in a position to catch the error before it affects your treatment.
compare with other therapies
We covered this comparison in full detail earlier in our conversation for the Talazoparib page — 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 |
Olaparib was first to market for this indication by about nine months, establishing the original proof-of-concept that PARP inhibition works in BRCA-mutated breast cancer specifically.
Efficacy — no significant difference in rigorous indirect comparison
- OlympiAD (olaparib): median PFS 7.0 months vs 4.2 months with chemotherapy (HR 0.58)
- EMBRACA (talazoparib): median PFS 8.6 months vs 5.6 months with chemotherapy (HR 0.54)
A Bayesian indirect treatment comparison found no significant difference in PFS between the two drugs, despite the numerically longer PFS with talazoparib — differences in trial populations between OlympiAD and EMBRACA mean direct number comparison requires statistical adjustment. Neither drug has shown a definitive overall survival advantage over chemotherapy in final analyses.
Side effects — talazoparib carries meaningfully higher myelosuppression
This is the most consistent, clinically meaningful difference. Talazoparib’s rates of serious cytopenias are notably higher:
- Grade ≥3 anemia: 39.2% with talazoparib
- 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 real practical difference
- Talazoparib: 1mg once daily
- Olaparib: 300mg twice daily (two 150mg tablets, twice daily)
Talazoparib’s once-daily regimen is a genuine convenience advantage for patients who prefer or need simpler dosing schedules.
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 setting where talazoparib doesn’t have equivalent established evidence. This distinction is particularly relevant if you’re being treated in the post-surgical setting rather than for metastatic disease.
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 based on rigorous indirect comparison, with the practical choice coming down to talazoparib’s once-daily 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 BRCA mutation, baseline blood counts, and dosing preferences.
How does testing work
We covered this mechanism in full detail earlier in our conversation — here are the key points pulled forward rather than repeating the research.
Cells have multiple DNA repair systems — two matter most here
DNA gets damaged constantly from normal metabolism, environmental exposures, and cell division. Two repair pathways are central to understanding PARP inhibition:
Homologous recombination repair (HRR) — a high-fidelity system repairing the most dangerous double-strand DNA breaks. BRCA1 and BRCA2 are essential proteins in this pathway, using an undamaged DNA copy as a template for accurate repair.
Base excision repair, involving PARP enzymes — a separate system repairing smaller, single-strand DNA damage. PARP1, PARP2, and PARP3 detect single-strand breaks and recruit other repair machinery to fix them.
What happens in a BRCA-mutated cell
A BRCA1 or BRCA2 mutation disables or severely impairs homologous recombination repair. The cell survives using other pathways including PARP-dependent repair for day-to-day damage. Because HRR is already broken, PARP-mediated repair becomes load-bearing — the cell depends on it more heavily than normal cells do.
How PARP inhibitors create the lethal combination — synthetic lethality
PARP inhibitors don’t simply block PARP’s enzymatic activity — they cause PARP to become physically trapped on DNA itself, forming PARP-DNA complexes that obstruct the replication machinery. As cells divide, these trapped complexes convert into double-strand breaks — and a BRCA-mutated cell, lacking functional HRR, has no reliable way to repair this damage. Accumulated unrepaired damage triggers cell death or catastrophic genomic instability.
This is called 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
Traditional chemotherapy damages DNA broadly across all dividing cells, causing widespread side effects. PARP inhibitors exploit a vulnerability that exists only in cells with a BRCA or HRR defect — which is why BRCA testing isn’t a formality but essential to identifying exactly which patients will benefit.
Why olaparib was first, and what followed
Olaparib was the original proof of concept that synthetic lethality works clinically — its FDA approval in 2014 established that selectively targeting BRCA-mutated tumors through PARP inhibition is both feasible and meaningfully effective. Talazoparib, rucaparib, and niraparib all followed, sharing the same core mechanism but with somewhat different PARP-trapping potency profiles.
Why resistance eventually develops
Resistance mechanisms include HRR pathway reactivation (the cancer cell partially restores homologous recombination function), reduced PARP trapping, and increased drug efflux. This explains why, after initial response, some BRCA-mutated cancers eventually progress — the cell population evolves around the vulnerability the drug was designed to exploit.
The bigger picture
PARP inhibitors represent precision medicine in the truest sense — not broadly toxic to fast-growing cells, but exploiting a specific genetic vulnerability that exists only in cells carrying a BRCA mutation or similar HRR defect. This is precisely why BRCA testing is non-negotiable before prescribing olaparib or talazoparib — without that underlying defect, the targeted lethal effect on cancer cells simply wouldn’t exist.
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.
