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Structural formula of maraviroc
Ball-and-stick model of the maraviroc molecule
Systematic (IUPAC) name
4,4-difluoro-N-{(1S)-3-[3-(3-isopropyl- 5-methyl-4H-1,2,4-triazol-4-yl)-8-azabicyclo[3.2.1]oct-8-yl]-1-phenylpropyl}cyclohexanecarboxamide
Clinical data
Trade names Selzentry
AHFS/ Monograph
MedlinePlus a607076
License data
  • AU: B1
  • US: B (No risk in non-human studies)
Routes of
Legal status
Legal status
Pharmacokinetic data
Bioavailability 23%[1]
Metabolism Liver
Biological half-life 16 h[2]
CAS Number 376348-65-1 YesY
ATC code J05AX09 (WHO)
PubChem CID 3002977
DrugBank DB04835 YesY
ChemSpider 20078004 N
NIAID ChemDB 104834
Chemical data
Formula C29H41F2N5O
Molar mass 513.666 g/mol
 NYesY (what is this?)  (verify)

Maraviroc (brand-named Selzentry, or Celsentri outside the U.S.) is an antiretroviral drug in the CCR5 receptor antagonist class used in the treatment of HIV infection. It is also classed as an entry inhibitor. It also appeared to reduce graft-versus-host disease in patients treated with allogeneic bone marrow transplantation for leukemia, in a phase 1/2 study.[3][4]

Mechanism of action[edit]

Maraviroc is an entry inhibitor. Specifically, maraviroc is a negative allosteric modulator of the CCR5 receptor, which is found on the surface of certain human cells. The chemokine receptor CCR5 is an essential co-receptor for most HIV strains and necessary for the entry process of the virus into the host cell. The drug binds to CCR5, thereby blocking the HIV protein gp120 from associating with the receptor. HIV is then unable to enter human macrophages and T-cells.[5] Because HIV can also use other coreceptors, such as CXCR4, an HIV tropism test such as a trofile assay must be performed to determine if the drug will be effective.[6]

Development and approval[edit]

Maraviroc, originally designated UK-427857, was developed by the drug company Pfizer in its UK labs located in Sandwich. On April 24, 2007 the U.S. Food and Drug Administration advisory panel reviewing maraviroc's New Drug Application unanimously recommended approval for the new drug,[7] and the drug received full FDA approval on August 6, 2007 for use in treatment experienced patients.[8]

On September 24, 2007, Pfizer announced that the European Commission approved maraviroc. Industry experts forecast annual maraviroc sales of $500 million by 2011.[9]


Two randomized, placebo-controlled clinical trials, known as MOTIVATE 1 & 2, compared 209 patients receiving optimized therapy plus a placebo to 426 patients receiving optimized therapy plus 150 mg maraviroc once daily and 414 patients receiving optimized therapy plus 150 mg maraviroc twice daily. At 48 weeks, 55% of participants receiving maraviroc once daily and 60% of participants receiving the drug twice daily achieved a viral load of less than 400 copies/mL compared with 26% of those taking placebo; about 44% of the once-daily and 45% of the twice-daily maraviroc group had a viral load of less than 50 copies/mL compared with about 23% of those who received placebo. In addition, those who received the entry inhibitor had a mean increase in CD4 cells of 110 cells/µL in the once-daily group, 106 cells/µL in the twice-daily group, and 56 cells/µL in the placebo group.[10][11][12]


The MOTIVATE trials showed no clinically relevant differences in safety between the maraviroc and placebo groups.[10]

Side effects[edit]

Maraviroc can cause serious, life-threatening side effects. These include liver problems, skin reactions, and allergic reactions. An allergic reaction may happen before liver problems occur.[13]

See also[edit]


  1. ^ Abel S, Russell D, Whitlock LA, Ridgway CE, Nedderman AN, Walker DK (April 2008). "Assessment of the absorption, metabolism and absolute bioavailability of maraviroc in healthy male subjects". British Journal of Clinical Pharmacology. 65 (Suppl 1): 60–7. doi:10.1111/j.1365-2125.2008.03137.x. PMC 2311408free to read. PMID 18333867. 
  2. ^ Abel S, Back DJ, Vourvahis M (2009). "Maraviroc: pharmacokinetics and drug interactions". Antiviral Therapy. 14 (5): 607–18. PMID 19704163. 
  3. ^
  4. ^ Blocade of lymphocyte chemotaxis in visceral graft-versus-host disease, Ran Reshef et al., New England Journal of Medicine, 367:135 (July 12, 2012)
  5. ^ Levy JA (January 2009). "HIV pathogenesis: 25 years of progress and persistent challenges". AIDS. 23 (2): 147–60. doi:10.1097/QAD.0b013e3283217f9f. PMID 19098484. 
  6. ^ Biswas P, Tambussi G, Lazzarin A (May 2007). "Access denied? The status of co-receptor inhibition to counter HIV entry". Expert Opinion on Pharmacotherapy. 8 (7): 923–33. doi:10.1517/14656566.8.7.923. PMID 17472538. 
  7. ^ Gay News From
  8. ^ Krauskopf, Lewis (August 6, 2007). "Pfizer wins U.S. approval for new HIV drug". Reuters. Retrieved 2007-08-06. 
  9. ^ Reuters, Europe gives final approval to Pfizer HIV drug
  10. ^ a b Stephenson J (April 2007). "Researchers buoyed by novel HIV drugs: will expand drug arsenal against resistant virus". JAMA. 297 (14): 1535–6. doi:10.1001/jama.297.14.1535. PMID 17426263. 
  11. ^ Emmelkamp JM, Rockstroh JK (October 2007). "CCR5 antagonists: comparison of efficacy, side effects, pharmacokinetics and interactions--review of the literature". European Journal of Medical Research. 12 (9): 409–17. PMID 17933722. 
  12. ^ "Maraviroc reduces viral load in naive patients at 48 weeks". AIDS Patient Care and STDs. 21 (9): 703–4. September 2007. PMID 17941136. 
  13. ^ AIDSinfo Drug Database: Maraviroc

External links[edit]