BevirimatFile:Bevirimat.svg

Clinical data
Synonyms| PA-457, 3-O-(3',3'-dimethylsuccinyl)- betulinic acid
Routes of
administration| Oral
Pharmacokinetic data
Metabolism| Hepatic glucuronidation (UGT1A3-mediated)
Elimination half-life| 56.3 to 69.5 hours
Identifiers

IUPAC name

* 3β-(3-carboxy-3-methyl -butanoyloxy)lup-20(29)- en-28-oic acid

CAS Number|

* 174022-42-5

PubChem CID|

* 457928

E number| {{#property:P628}}
ECHA InfoCard| {{#property:P2566}}Lua error in Module:EditAtWikidata at line 36: attempt to index field 'wikibase' (a nil value).
Chemical and physical data
Formula| C36H56O6
Molar mass| 584.826 g/mol
3D model (JSmol)|

* Interactive image

SMILES

* CC(=C)C1CCC2(C1C3CCC4C5(CCC(C(C5CCC4(C3(CC2)C)C)(C)C)OC(=O)CC(C)(C)C(=O)O)C)C(=O)O

Bevirimat is a anti-HIV drug derived from a betulinic acid-like compound, first isolated from Syzygium claviflorum, a Chinese herb. It is believed to inhibit HIV by a novel mechanism, so-called maturation inhibition. [1] It is not currently FDA-approved, but is undergoing clinical trials conducted by the pharmaceutical company Panacos.

## Contents

* 1 Clinical trials
* 2 Pharmacokinetics
* 3 Mechanism of action
* 4 External links
* 5 References
* 6 External links

## Clinical trials[edit | edit source]

In December 2007, some results of the Phase IIb trial were released. Thomson Financial News reported that, "some patients respond 'very well' to the drug, while another population 'does not respond as well at current dose levels.'" Panacos said it intends to add a group to the study at a higher dosage.[2]

## Pharmacokinetics[edit | edit source]

According to the only currently available study, "the mean terminal elimination half-life of bevirimat ranged from 56.3 to 69.5 hours, and the mean clearance ranged from 173.9 to 185.8 mL/hour." [3]

## Mechanism of action[edit | edit source]

Bevirimat targets the gag polyprotein precursor, the main structural protein responsible for assembly and budding of virion particles.[4] By binding to the gag polyprotein, bevirimat prevents its cleavage by the protease enzyme into functional subunits. Unlike the protease inhibitors, bevirimat binds the gag protein, not the protease enzyme. The resulting virus particles are structurally defective and are incapable of spreading infection around the body.[5] For unknown reasons, protease inhibitor-resistant HIV-1 was hypersensitive to bevirimat in vitro.[6]

## External links[edit | edit source]

* An animation illustrating Bevirimat's mechanism of action
* Overview and Publication Listing for Bevirimat from Panacos

## References[edit | edit source]

1. ↑ Smith PF, Ogundele A, Forrest A, Wilton J, Salzwedel K, Doto J, Allaway GP, Martin DE. Phase I and II study of the safety, virologic effect, and pharmacokinetics/pharmacodynamics of single-dose 3-o-(3',3'-dimethylsuccinyl)betulinic acid (bevirimat) against human immunodeficiency virus infection. Antimicrob Agents Chemother. 2007 Oct;51(10):3574-81. Epub 2007 Jul 16. PMID 17638699
2. ↑ Zhou, Wanfeng. Panacos: Bevirimat data support further dose escalation. Thomson Financial News. 10 Dec 2007.
3. ↑ Martin DE, Blum R, Doto J, Galbraith H, Ballow C (2007). "Multiple-dose pharmacokinetics and safety of bevirimat, a novel inhibitor of HIV maturation, in healthy volunteers". Clin Pharmacokinet. 46 (7): 589–98. PMID 17596104.CS1 maint: Multiple names: authors list (link)
4. ↑ Salzwedel K, Martin DE, Sakalian M (2007). "Maturation inhibitors: a new therapeutic class targets the virus structure". AIDS Rev. 9 (3): 162–72. PMID 17982941.CS1 maint: Multiple names: authors list (link)
5. ↑ bevirimat (PA-457). Panacos Pharmaceuticals Inc. accessed 28 Dec 2007.
6. ↑ Stoddart CA, Joshi P, Sloan B; et al. (2007). "Potent Activity of the HIV-1 Maturation Inhibitor Bevirimat in SCID-hu Thy/Liv Mice". PLoS ONE. 2 (11): e1251. doi:10.1371/journal.pone.0001251. PMID 18043758.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)

## External links[edit | edit source]

* AIDSmeds Bevirimat

* v
* t
* e

Antivirals used against HIV (HAART) (primarily J05)

Nucleoside & Nucleotide
Reverse Transcriptase
Inhibitors (NRTI)|

Abacavir (ABC)° • Emtricitabine° • Lamivudine (3TC)° • Tenofovir° • Didanosine • Zidovudine (AZT) • Apricitabine† • Stampidine† • Elvucitabine† • Racivir† • Amdoxovir† • Stavudine‡ • Zalcitabine‡

Non-Nucleoside
Reverse Transcriptase
Inhibitors (NNRTI)|

Efavirenz° • Nevirapine • Etravirine • Rilpivirine† • Loviride‡ • Delavirdine‡

Protease Inhibitors (PI)|

Atazanavir° • Fosamprenavir° • Lopinavir° • Darunavir • Nelfinavir • Ritonavir • Saquinavir • Tipranavir • Amprenavir‡ • Indinavir‡

Entry/fusion inhibitors|

Enfuvirtide • Maraviroc • Vicriviroc† • PRO 140† • Ibalizumab†

Integrase inhibitors|

Raltegravir • Elvitegravir†

Maturation inhibitors|

Bevirimat† • Vivecon™†

Combined formulations|

Combivir • Atripla • Trizivir • Truvada • Kaletra • Epzicom

Other &
experimental agents|

Foscarnet • Hydroxyurea • Synergistic enhancers • Epigallocatechin gallate • Portmanteau inhibitors • Globoidnan A • Griffithsin • Diarylpyrimidines • Calanolide A • Cyanovirin-N • Miltefosine

°DHHS preferred first-line agent. †Undergoing clinical trials, not FDA approved. ‡Formerly or rarely used agent.

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