Pralatrexatum

Pralatrexatum Uses, Dosage, Side Effects, Food Interaction and all others data.

Pralatrexatum is an antimetabolite for the treatment of relapsed or refractory peripheral T-cell lymphoma. It is more efficiently retained in cancer cells than methotrexate. FDA approved on September 24, 2009.

Pralatrexatum is a 10-deazaaminopterin analogue of methotrexate. Compared to methotrexate, pralatrexate binds to RTC-1 with 10-times the affinity and is a more potent substrate for FPGS. As a result, pralatrexate is better internalized and retained in cancer cells and is more cytotoxic.Km, pralatrexate = 0.3 μmol/L;Km, methotrexate = 4.8 μmol/L;Vmax/Km (rate of intracellular transport), pralatrexate = 12.6Vmax/Km (rate of intracellular transport), methotrexate = 0.9

Pralatrexatum
Uses
Dosage
Side Effect
Precautions
Interactions
Uses during Pregnancy
Uses during Breastfeeding
Accute Overdose
Food Interaction
Half Life
Volume of Distribution
Clearance
Interaction With other Medicine
Contradiction
Storage

Trade Name	Pralatrexatum
Availability	Prescription only
Generic	Pralatrexate
Pralatrexate Other Names	Pralatrexate, Pralatrexato, Pralatrexatum
Related Drugs	prednisone, methotrexate, dexamethasone, rituximab, Rituxan, Revlimid, cyclophosphamide, vincristine, Imbruvica, Velcade
Type
Formula	C₂₃H₂₃N₇O₅
Weight	Average: 477.4726 Monoisotopic: 477.176066881
Protein binding	67 - 86% bound to plasma protein, albumin is the major binder. Does not significantly displace substrates from proteins.
Groups	Approved, Investigational
Therapeutic Class
Manufacturer
Available Country
Last Updated:	September 19, 2023 at 7:00 am

Uses

Pralatrexatum is an antineoplastic agent used for the treatment of relapsed or refractory peripheral T-cell lymphoma.

Treatment of relapsed or refractory peripheral T-cell lymphoma.

Pralatrexatum is also used to associated treatment for these conditions: Cutaneous T-Cell Lymphoma (CTCL), Relapsed Peripheral T-Cell Lymphoma, Refractory Peripheral T-cell Lymphoma Unspecified

How Pralatrexatum works

The selectivity of pralatrexate for cancer cells is based upon the observation that cancer cells generally have an overexpression of reduced folate carrier protein-1 (RTC-1) compared to normal somatic cells. This carrier protein allows the entrance of pralatrexate into the cell. Upon entering the cell, folypolyglutamate synthase FPGS catalyzes the polyglutamination of pralatrexate so that it is retained inside the cell.
Once inside, pralatrexate competitively inhibits dihydrofolate reductase (DHFR) and thymidylate synthase. Subsequent depletion of thymidine monophosphate (TMP) occurs so that the cancer cell is unable to synthesize DNA and RNA. As a result, the cancer cell cannot proliferate and is forced to undergo apoptosis. Pralatrexatum is more effective against cells that are actively dividing.

Toxicity

Mucositis is the dose-limiting toxicity. Folic acid and vitamin B12 supplements do not prevent mucositis from happening.

Food Interaction

No interactions found.

Pralatrexatum Drug Interaction

Moderate: ibuprofen / pseudoephedrine, filgrastim, bifidobacterium infantis / lactobacillus acidophilus / streptococcus thermophilus, denosumabUnknown: fexofenadine / pseudoephedrine, diphenhydramine, menthol topical, fulvestrant, ginger, palbociclib, dextromethorphan / guaifenesin, esomeprazole, lansoprazole, chondroitin / glucosamine, levothyroxine, riboflavin, ascorbic acid, ergocalciferol, zinc sulfate, cetirizine

Pralatrexatum Disease Interaction

Moderate: liver impairment, renal impairment

Volume of Distribution

Vss, R-pralatrexate = 37 L Vss, S-pralatrexate = 105 L

Elimination Route

Pralatrexatum demonstrates linear pharmacokinetics with a multiphasic decline with both diasteromers over dose range of 30-325 mg/m^2. Bioavailability, nonformulated preparation = 13 - 20%