What cancer is erlotinib used for?

What cancer is erlotinib used for?

Erlotinib is used to treat certain types of non-small cell lung cancer that has spread to nearby tissues or to other parts of the body in patients who have already been treated with at least one other chemotherapy medication and have not gotten better.

Is erlotinib a chemotherapy drug?

Erlotinib is a non-chemotherapy drug for the treatment of advanced or metastatic NSCLC and is administered orally once a day. It successfully inhibits EGFR, a protein involved in the growth and development of cancers.

What is the brand name for erlotinib?

Tarceva is the trade name for the generic drug name Erlotinib. In some cases, health care professionals may use the trade name Tarceva when referring to the generic drug name Erlotinib.

Which type of cancer is erlotinib most often prescribed to treat?

Erlotinib (Tarceva®) is used to treat non-small cell lung cancer (NSCLC) and pancreatic cancer. It may sometimes be used to treat other cancers.

Can erlotinib cure lung cancer?

Currently, erlotinib, at a standard oral daily dose of 150 mg, is licensed for the treatment of unselected recurrent non-small cell lung cancer (NSCLC) patients, however, it is being investigated in all stages of NSCLC. Erlotinib is well tolerated, with common toxicities including rash and diarrhoea.

Which of the following is a known side effect of erlotinib?

Diarrhea, dry skin, muscle/joint pain, mouth sores, unusual eyelash growth, or eye dryness/redness/irritation may occur. Diarrhea can be severe. In some cases, your doctor may prescribe medication to relieve diarrhea. If any of these effects last or get worse, tell your doctor or pharmacist promptly.

How long does erlotinib work?

What is erlotinib resistance? Erlotinib is highly effective in the subset of patients carrying EGFR mutations. However, even these patients will eventually begin to show progression of their cancer after about 12 months of erlotinib therapy.

What erlotinib inhibits?

Erlotinib is an inhibitor of the epidermal growth factor receptor (EGFR) tyrosine kinase that is used in the treatment of non-small cell lung cancer, pancreatic cancer and several other types of cancer. It is typically marketed under the trade name Tarceva.

What causes resistance to erlotinib?

The most common mechanism of acquired resistance is due to emergence of T790M mutation, approximately 50% of NSCLC patients develop resistance to TKIs [31, 32]. Potential mechanism by which T790M causes resistance to EGFR-TKIs is by increasing the affinity to ATP [9, 33].

What is the new lung cancer drug?

Today, the U.S. Food and Drug Administration approved Lumakras (sotorasib) as the first treatment for adult patients with non-small cell lung cancer whose tumors have a specific type of genetic mutation called KRAS G12C and who have received at least one prior systemic therapy.

What are the side effects of Tarceva?

Where does erlotinib bind?

Erlotinib binds to the epidermal growth factor receptor (EGFR) tyrosine kinase in a reversible fashion at the adenosine triphosphate (ATP) binding site of the receptor.

How do you treat erlotinib rash?

Erlotinib-related xeroderma should be treated with emollients, with the addition of a topical steroid (at least strong class) for grade 2 severity or higher (Table I). Patients should be switched to a medium-class topical steroid once symptoms improve.

What is the cost of erlotinib?

The cost for erlotinib oral tablet 100 mg is around $5,656 for a supply of 30 tablets, depending on the pharmacy you visit. Prices are for cash paying customers only and are not valid with insurance plans.

Does Tarceva shrink tumors?

Most patients respond to Tarceva, their tumors shrinking or even becoming undetectable. However, this effect is temporary. Most tumors come back, and most of them are ‘equipped’ with a new mutation in EGFR, known as T790M.

Why do people develop resistance to erlotinib?

Resistance to treatment In the case of erlotinib this typically occurs 8–12 months from the start of treatment. Over 50% of resistance is caused by a mutation in the ATP binding pocket of the EGFR kinase domain involving substitution of a small polar threonine residue with a large nonpolar methionine residue (T790M).

How does T790M resistance occur?

The most common resistance mechanism results from the development of the so-called ‘gatekeeper’ T790M mutation in EGFR exon 20, which sterically hinders the binding of first- and second-generation TKIs to the ATP-binding site of EGFR.