Address
Sector 14, Road no. 18, Uttara, 1230
Dhaka, Bangladesh
Rx Prescripttion Only-YMYL Medical Content
Olanib 150 mg
Olaparib 150mg tablets – Everest Pharmaceuticals 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 to receive FDA approval — established the entire PARP inhibitor drug class
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
Anemia, neutropenia, and thrombocytopenia are common — baseline complete blood count is required before starting, with regular monitoring throughout treatment, particularly in the first months.
Moderate renal impairment (CrCl 31-50 mL/min) requires dose reduction to 200mg twice daily. Olaparib has not been adequately studied in severe renal impairment — confirm your kidney function before starting.
4
Discuss MDS/AML risk and long-term monitoring plan
Myelodysplastic syndrome and acute myeloid leukemia have occurred — a small but serious long-latency risk shared across the PARP inhibitor class. Discuss what ongoing blood count monitoring looks like for the full duration of treatment.
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, establishing a completely new approach to BRCA-related cancer that’s since been extended across four cancer types. The SOLO-1 results in BRCA-mutated ovarian cancer maintenance were genuinely striking — 70% reduction in progression risk and 60% still progression-free at three years represent outcomes that changed how we think about what maintenance therapy can achieve. The MDS/AML risk is rare but has a long latency, which shapes how I counsel patients about ongoing monitoring even after years of treatment.”
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
Here are key questions to bring to your oncologist — given that olaparib spans four different cancer types with somewhat different clinical contexts for each, confirming exactly which indication applies and which specific biomarker testing has been done is the most important starting point.
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 for this drug
- 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 — the most important ongoing surveillance
- 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 the MDS/AML risk — rare but long-latency
- How is this risk explained in terms of actual likelihood for someone in my situation?
- What ongoing blood count monitoring is specifically designed to watch for this, and for how long — given that it can develop months to years into treatment?
- What symptoms outside of scheduled blood tests should prompt me to flag something?
- If I’ve had prior chemotherapy, does that change my risk or monitoring intensity?
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
- What imaging or biomarker testing will track whether this is working?
- How soon might we expect to see signs of response, or for maintenance therapy, how will disease stability be confirmed?
About the longer road
- 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 for each other on a milligram-to-milligram basis due to different bioavailability, it’s worth confirming explicitly with your pharmacist each time you refill which formulation you’ve been prescribed, since inadvertently receiving the wrong formulation could mean getting either too much or too little drug even if the milligram number looks similar.
compare with other therapies
We covered this comparison in detail earlier in our conversation for the Talaparib page — here are the key findings pulled forward rather than repeating the research.
Both are PARP inhibitors targeting the same biological vulnerability
| Olaparib (Lynparza) | Talazoparib (Talzenna) | |
|---|---|---|
| FDA approval (breast) | January 2018 — first PARP inhibitor approved for breast cancer | October 2018 |
| Dosing | 300mg twice daily | 1mg once daily |
| Manufacturer | AstraZeneca/Merck | Pfizer |
| Pivotal trial | OlympiAD | EMBRACA |
Olaparib has the distinction of being first to market for this indication by about nine months, making it the original proof-of-concept that PARP inhibition works in BRCA-mutated breast cancer specifically.
Efficacy — no significant difference in the rigorous comparison
Both drugs showed comparable PFS improvements over chemotherapy in their respective trials:
- 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 fixed-effects indirect treatment comparison specifically analyzing both trials found no significant difference in PFS between olaparib and talazoparib — though differences in specific adverse events were identified. Neither drug has shown a definitive overall survival advantage over chemotherapy in final analyses.
Cross-trial comparison numbers might suggest talazoparib has a numerical edge, but this is precisely the kind of comparison that requires statistical adjustment for differing trial populations — the rigorous indirect comparison found no meaningful efficacy difference.
Side effects — where the meaningful differences actually live
Myelosuppression appears to be a class effect, but talazoparib’s rates are notably higher:
- 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
Talazoparib’s higher myelosuppression rates are the most consistent, clinically meaningful difference between the two drugs — a patient with pre-existing anemia, borderline blood counts, or concern about cytopenias might 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 struggle with twice-daily medication adherence.
Early-stage disease — olaparib has an additional, established evidence base
The OlympiA trial established olaparib’s role as adjuvant therapy after surgery in high-risk early-stage BRCA-mutated breast cancer — a setting where talazoparib doesn’t currently have the same established evidence. If you’re being treated in the early-stage, post-surgical setting rather than metastatic disease, this distinction is particularly relevant.
Guideline positioning
Both are NCCN Category 1 recommendations for metastatic BRCA-mutated HER2-negative breast cancer — neither is considered inferior from a guideline standpoint. The choice is increasingly framed as a tolerability and practical-factors decision rather than an efficacy-driven one.
Bottom line
Talazoparib and olaparib are formally equivalent in their ability to suppress BRCA-mutated breast cancer based on the best available indirect comparison. The real decision comes down to: talazoparib’s once-daily dosing convenience versus olaparib’s more established and somewhat better-tolerated myelosuppression profile, plus olaparib’s additional well-established role in earlier-stage disease. This is worth a direct conversation with your oncologist about your specific BRCA mutation, blood count baseline, and personal preferences around dosing frequency.
How does testing work
We covered this mechanism in detail earlier in our conversation for the Talaparib page — here are the key points pulled forward rather than repeating the research.
The basic biology — cells have multiple DNA repair systems
DNA gets damaged constantly from normal metabolism, environmental exposures, and cell division. Cells have evolved multiple overlapping repair pathways because relying on just one system would be too risky. Two are most relevant here:
Homologous recombination repair (HRR) — a high-fidelity system that repairs the most dangerous type of DNA damage, double-strand breaks. BRCA1 and BRCA2 are essential proteins in this pathway. It’s considered high-fidelity because it uses an undamaged copy of the DNA sequence as a template, ensuring accurate repair without introducing new errors.
Base excision repair, involving PARP enzymes — a separate system that repairs smaller, single-strand DNA damage. PARP1 and PARP2 detect single-strand breaks and recruit other repair machinery to fix them.
What happens in a BRCA-mutated cell
A person with a BRCA1 or BRCA2 mutation has cells with a disabled or severely impaired homologous recombination repair pathway. The cell can still survive using other pathways, including PARP-dependent repair, to handle most day-to-day damage. Because HRR is already broken, PARP-mediated repair becomes load-bearing — the cell relies on it more heavily than normal cells do.
How PARP inhibitors create the lethal combination — synthetic lethality
PARP inhibitors don’t just block PARP’s enzymatic activity — they cause PARP to become “trapped” on DNA itself, forming PARP-DNA complexes that physically obstruct the DNA replication machinery. As cells try to divide, these trapped complexes get converted into double-strand breaks during replication — and a BRCA-mutated cell, lacking functional HRR, has no reliable way to fix that double-strand damage. Accumulated, unrepaired damage triggers cell death or catastrophic genomic instability.
This is genuinely called “synthetic lethality” — the drug becomes lethal specifically when combined with the pre-existing BRCA defect, while normal cells with healthy HRR can tolerate PARP inhibition largely in stride.
Why this is more targeted than chemotherapy
Traditional chemotherapy damages DNA broadly across all dividing cells, which is why it causes 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 the first, and what followed
Olaparib was the original proof of concept that this synthetic lethality strategy 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, each with somewhat different potency and PARP-trapping efficiency profiles but sharing the same core synthetic lethality mechanism.
Why resistance eventually develops
Resistance mechanisms include HRR pathway reactivation (the cancer cell finds a way to partially restore homologous recombination function), reduced PARP trapping, and increased drug efflux through pumps that expel the drug before it can act. This explains why, after initial response, some BRCA-mutated cancers eventually progress — the cancer cell population evolves around the very 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 drug simply wouldn’t have the same targeted lethal effect on a patient’s cancer cells.
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.
