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- PARP inhibitors: used for high grade serous ovarian cancer
- Bevacizumab: used for high grade serous ovarian cancer
- MEK inhibitors: used for low grade serous ovarian cancer
- Where can I get more support?
Drugs such as PARP inhibitors, bevacizumab and MEK inhibitors are known as targeted treatments because they target the things about a cancer cell that make it different from a normal cell. You may also hear them called maintenance treatments. That’s because they aim to increase the amount of time that the cancer remains inactive. This is when the cancer stops growing.
You may be offered targeted cancer treatments after chemotherapy. This will depend on:
- the type of ovarian cancer you have
- whether surgery is possible
- if your cancer responded well to chemotherapy.
The way drugs are approved for use in the NHS differs across the UK. This means that there can be some differences in which drugs are available depending on where you live. If you have questions about whether a drug might work for you, or about why you have - or haven’t - been offered one, speak to your clinical team. You can also call our nurse-led support line on 0808 802 6000.
PARP inhibitors
What are PARP inhibitors?
PARP inhibitors are drugs that are used to stop cancer cells from repairing themselves, so the cancer cells die. They aim to reduce the chance of the cancer coming back or delay it coming back.
There are three PARP inhibitors available in the UK for ovarian cancer:
- olaparib (Lynparza®)
- niraparib (Zejula®)
- rucaparib (Rubraca®)
These are all given as tablets you take at home. You can receive a PARP inhibitor if you have stage 3 or 4 high-grade epithelial ovarian cancer, fallopian tube cancer or primary peritoneal cancer that has responded to platinum-based chemotherapy (usually carboplatin or cisplatin and paclitaxel).
You can usually only access PARP inhibitors once. So if you had PARP inhibitor treatment after your first course of chemotherapy, you won’t usually be offered another one. This is because you're less likely to have a response to a PARP inhibitor if you have had one already.
Which ones you're eligible for and at what stage of your treatment depends on:
- your personal situation,
- whether you have a BRCA1 or 2 gene variant or
- whether your tumour tests positive for homologous recombination deficiency (HRD).
Use our helpful tool below to find out which PARP inhibitors you may be able to access.
- Why does having a BRCA gene variant make a difference?
Your body is made up of tiny building blocks called cells. Each cell contains DNA (deoxyribonucleic acid). DNA is like an instruction manual which tells your cells how to work and behave.
Sections of your DNA are known as genes. Genes are instructions for different parts of your body such as your eye colour. They also help keep your cells healthy.
Sometimes genes have small changes in their DNA. These are known as gene variants. Certain gene variants can increase the risk of developing cancer compared to people who don’t have the genetic variant. BRCA1 and BRCA2 gene variants are linked to an increased risk of ovarian and breast cancer.
BRCA1 and BRCA2 genes normally help cells repair breaks in DNA. Changes to these genes mean that cancer cells are less able to repair DNA damage. PARP inhibitors work by further blocking cells’ ability to repair damage. These drugs are more likely to work well in those with BRCA1 or BRCA2 variants because the cancer cells are already less able to repair their DNA. This means that cancer cells are less likely to repair themselves and grow.
- Why does being HRD positive make a difference?
Cells are constantly repairing damage to their DNA. One process to repair cells' DNA is called homologous recombination. Homologous recombination deficiency (HRD) is when the homologous recombination process isn’t working. This means that those cells are less able to repair damage in their DNA.
Being HRD positive means you may have access to more PARP inhibitor options and they may work more effectively. This is because PARP inhibitors work by blocking a different DNA repair process. Since HRD positive cells are already less able to repair their DNA, PARP inhibitors are more likely to work well on cells that are HRD positive because cancer cells are less likely to repair damage in their DNA and grow.
