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Category Antiviral
Catalog number BBF-05849
CAS 4428-95-9
Molecular Weight 126.01
Molecular Formula CH3O5P
Purity 95%

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Foscarnet is a pyrophosphate analog DNA polymerase inhibitor that has activity against several viruses, but is primarily used to treat CMV retinitis. Because it can cross the blood-brain barrier, it can be used to treat viral infections of the central nervous system.


Related CAS 63585-09-1 (trisodium salt) 34156-56-4 (hexahydrate)
Synonyms Phosphonoformate; Carboxyphosphonic acid; Foscarmet; Phosphonocarboxylic acid; Dihydroxyphosphinecarboxylic acid oxide; Phosphonomethanoic acid; Dihydroxyphosphanecarboxylic acid oxide; Phgosphonocarboxylic acid; NSC313410; Phosphinecarboxylic acid, 1,1-dihydroxy-, 1-oxide; Foscamet
Storage Store at 2-8°C
IUPAC Name phosphonoformic acid
Canonical SMILES C(=O)(O)P(=O)(O)O
InChI InChI=1S/CH3O5P/c2-1(3)7(4,5)6/h(H,2,3)(H2,4,5,6)


Antibiotic Activity Spectrum Viruses
Boiling Point 490.7±28.0°C at 760 mmHg
Density 2.142±0.1 g/cm3

Reference Reading

1.Treatment of CMV Infection after Allogeneic Hematopoietic Stem Cell Transplantation.
Maffini E1,2, Giaccone L1,2, Festuccia M1,2, Brunello L1,2, Busca A1, Bruno B1,2. Expert Rev Hematol. 2016 Apr 4. [Epub ahead of print]
Despite a remarkable reduction in the past decades, cytomegalovirus (CMV) disease in allogeneic hematopoietic stem cell transplant (HSCT) recipients remains a feared complication, still associated with significant morbidity and mortality. Today first line treatment of CMV infection/reactivation is still based on dated antiviral compounds Ganciclovir (GCV), Foscarnet (FOS) and Cidofovir (CDF) with their burdensome weight of side effects. Maribavir (MBV), Letermovir (LMV) and Brincidofovir (BDF) are three new promising anti-CMV drugs without myelosuppressive properties or renal toxic effects that are under investigation in randomized phase II and III trials. Adoptive T-cell therapy (ATCT) in CMV infection possesses a strong rationale, demonstrated by several proof of concept studies; its feasibility is currently under investigation by clinical trials. ATCT from third-party and naïve donors could meet the needs of HSCT recipients of seronegative donors and cord blood grafts.
2.Successful treatment with foscarnet for ganciclovir-resistant cytomegalovirus infection in a kidney transplant recipient: A case report.
Iwami D1, Ogawa Y2, Fujita H3, Morita K1, Sasaki H1, Oishi Y1, Higuchi H1, Hatanaka K3, Shinohara N1. Nephrology (Carlton). 2016 Mar 10. doi: 10.1111/nep.12767. [Epub ahead of print]
Cytomegalovirus (CMV) infection is the most common infectious complication following solid organ transplantation. Ganciclovir (GCV)-resistant CMV infection may be fatal, and is difficult to treat whilst avoiding allograft rejection. A 31-year-old woman received a second ABO-incompatible kidney transplant, from her father. Induction therapy consisted of basiliximab and rituximab followed by maintenance immunosuppression with tacrolimus, mycophenolate mofetil, and methylprednisolone. Her CMV serostatus was D+ /R- at second transplant and she received prophylactic low-dose valganciclovir (VGCV). BK polyoma virus nephropathy (BKVN) developed 7 months after transplant concurrent with CMV hepatitis and retinitis. VGCV was increased to a therapeutic dose combined with reduced immunosuppression with minimal methylprednisolone (2 mg/day) and everolimus (0.5 mg/day). However, pp65 antigenemia continued to increase for 6 weeks. Her CMV was defined as ganciclovir (GCV)-resistant.
3.Human cytomegalovirus antiviral drug resistance in hematopoietic stem cell transplantation: current state of the art.
Campos AB1,2, Ribeiro J1,3,2, Boutolleau D4,5,6, Sousa H1,3. Rev Med Virol. 2016 Mar 14. doi: 10.1002/rmv.1873. [Epub ahead of print]
Human cytomegalovirus (HCMV) infection is a major cause of morbidity and mortality in allogeneic hematopoietic stem cell transplant recipients. The significant clinical impact of HCMV infection and progression to HCMV disease among allogeneic hematopoietic stem cell transplant recipients has been reduced by prophylactic, preemptive, and curative treatments using ganciclovir, valganciclovir, foscarnet, and cidofovir. Resistance to (val)ganciclovir results from mutations localized in HCMV UL97 gene (encoding the pUL97 phosphotransferase), UL54 gene (encoding the pUL54 DNA polymerase), or both genes, whereas foscarnet and cidofovir resistance results from mutations localized within UL54 gene only. This review is focused on HCMV antiviral drug resistance, including the functions of target genes of antivirals, the mechanisms of antiviral resistance, the different mutations in pUL97 and pUL54 that have been identified in either clinical isolates or laboratory strains, and their impact on HCMV susceptibility to antiviral drugs.
4.Identification of resistance-associated HCMV UL97- and UL54-mutations and a UL97-polymporphism with impact on phenotypic drug-resistance.
Fischer L1, Imrich E1, Sampaio KL2, Hofmann J3, Jahn G1, Hamprecht K1, Göhring K4. Antiviral Res. 2016 Apr 4. pii: S0166-3542(16)30087-0. doi: 10.1016/j.antiviral.2016.04.002. [Epub ahead of print]
BACKGROUND: Human cytomegalovirus (HCMV) drug-resistance remains of high clinical importance. While UL97-mutations can confer ganciclovir-resistance, UL54-mutations can be associated with resistance to ganciclovir, foscarnet and/or cidofovir.

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