Nuparp 200mg tablet

Yes, it's safe; administering rucaparib tablet to patients with kidney disease is deemed safe, and no dose adjustments are required. However, it is advisable to inform your physician of any existing kidney disorders before commencing the therapy.

Yes, male patients with female partners of reproductive potential are advised to utilize effective contraception throughout the treatment and for a period of 3 months following the last dose of rucaparib tablets.

Provide your doctor with comprehensive details regarding your medical and medication history, encompassing over-the-counter medicines as well as nutritional or vitamin supplements that you are currently using.

Yes, this medication increases your skin's sensitivity to sunlight. Consult your doctor and, if advised, use sunscreen diligently throughout the treatment.

The duration of your treatment depends on your disease condition and severity. Your doctor will decide your dose and the duration of your treatment.

Rucaparib mechanism of action

Rucaparib works by stopping poly(ADP-ribose) polymerase (PARP), an important enzyme in DNA repair processes. The key steps in the mechanism of action of Rucaparib are as follows: 1. PARP Inhibition: Rucaparib is classified as a PARP inhibitor. PARP enzymes play a vital role in repairing damaged DNA within cells. When a cell experiences DNA damage, PARP is activated to facilitate the repair process. 2. Synthetic Lethality: In cancer cells, particularly those with specific genetic mutations such as BRCA mutations, the DNA repair mechanisms are already compromised. By inhibiting PARP, Rucaparib induces a state of synthetic lethality. This means that cancer cells, which already have impaired DNA repair, become even more vulnerable to the inhibition of PARP, leading to increased DNA damage. 3. Preventing DNA Repair in Cancer Cells: As Rucaparib suppresses PARP activity, cancer cells, especially those with defective DNA repair pathways, are unable to effectively repair DNA damage. This results in the accumulation of DNA lesions within the cancer cells. 4. Cell Death: The accumulation of unrepaired DNA damage ultimately leads to the activation of programmed cell death mechanisms, such as apoptosis, in the cancer cells. This process selectively targets cancer cells while sparing normal, healthy cells that have functional DNA repair mechanisms. 5. Targeting BRCA-Mutated Cancers: Rucaparib's mechanism of action is particularly significant in cancers with BRCA mutations. These mutations render cancer cells more reliant on alternative DNA repair pathways, such as PARP-mediated repair. Because Rucaparib stops PARP from working, it takes advantage of this weakness to target and kill BRCA-mutated cancer cells. In summary, Rucaparib's mechanism of action revolves around inhibiting PARP, disrupting DNA repair processes in cancer cells, and exploiting the inherent vulnerabilities, especially in those with BRCA mutations. This targeted approach represents a significant advancement in precision medicine for the treatment of certain cancers.