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Sustiva (Efavirenz)

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Sustiva is used to treat HIV infection in combination with other anti-HIV medications. If Sustiva is the only drug you take to treat HIV infection, it may stop working.

Other names for this medication:
Adiva, Avifanz, Aviranz, Ciplaefavir, Efatec, Efavir, Efavirenz, Efavirenzum, Filginase, Stocrin, Stocrit, Sulfinav, Virorrever, Virzen, Efcure, Efferven, Efamat, Viranz, Effahope, Evirenz, Estiva

Similar Products:
Combivir, Epivir, Retrovir, Zerit, Viramune, Viramune XR, Rescriptor, Delavirdine, Nevirapine, Edurant, Truvada, Atripla, Norvir , Isentress, Prezista, Reyataz, Complera, Epzicom, Stribild, Epivir, Kaletra, Viread, Intelence, lamivudine, Ziagen, Ritonavir, Abacavir , Raltegravir, Tenofovir, Tivicay, Crixivan

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Also known as:  Efavirenz.


Sustiva is used to treat HIV infection in combination with other anti-HIV medications. If Sustiva is the only drug you take to treat HIV infection, it may stop working.

Sustiva is an oral medication that is used for the treatment of infections with the human immunodeficiency virus (HIV). It is similar to nevirapine (Viramune) and delavirdine (Rescriptor).

Sustiva is also known as Efavirenz, Stocrin.

Sustiva is in a class of drugs called reverse transcriptase inhibitors which also includes zalcitabine (Hivid), zidovudine (Retrovir), didanosine (Videx), and lamivudine (Epivir). During infection with HIV, the HIV virus multiplies within the body's cells. The newly-formed viruses then are released from the cells and spread throughout the body where they infect other cells. In this manner, the infection continually spreads to new, uninfected cells that the body is continually producing, and HIV infection is perpetuated. When producing new viruses, the HIV virus must manufacture new DNA for each virus. Reverse transcriptase is the enzyme that the virus uses to form this new DNA. Sustiva directly inhibits the activity of reverse transcriptase and blocks the production of DNA and new viruses. Unlike zidovudine, efavirenz does not need to be converted to an active form. Sustiva does not kill existing HIV virus and it is not a cure for HIV.


Take this drug by mouth, generally once daily as directed. Take on an empty stomach with a glass of water. Taking Sustiva with food, especially a high-fat meal can lead to increased blood levels of the drug and increase your risk of having side effects.

Best taken at bedtime during the first month of use. Using this drug regularly at bedtime may decrease certain side effects. Use this medication regularly in order to get the most benefit from it. To help you remember, use it at the same time each day. Do not take more or less of this drug than prescribed, or stop taking it unless directed to do so by your doctor. Read the patient information leaflet provided by your pharmacist.

If you want to achieve most effective results do not stop taking Sustiva suddenly.


If you overdose Sustiva and you don't feel good you should visit your doctor or health care provider immediately.


Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture and heat. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Sustiva are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.


Do not take Sustiva if you are allergic to Sustiva components.

Do not take Sustiva if you are pregnant, planning to become pregnant, or are breast-feeding. It is unknown if Sustiva is excreted in breast milk. Avoid breast-feeding because breast milk can transmit HIV.

Be careful with Sustiva if you have mental disorders, liver disease (such as hepatitis).

Avoid machine driving.

Limit alcohol intake, as it may intensify drug side effects.

It can be dangerous to stop Sustiva taking suddenly.

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Efavirenz was administered with one or more novel NRTIs to 55 patients (27 antiretroviral-naive and 28 patients experienced with NRTIs only), compared with 52 patients who needed a multidrug salvage regimen after two or more failures of a 15-40 month PI-containing regimen. In an intention-to-treat analysis, con-sidering early interruption or an unsatisfactory virological course as a failure, only one patient on salvage therapy completed a favourable 15 month follow-up, compared with 31 patients experiencing first-line efavirenz-based HAART (P < 0.0001). The immunological response was less affected in both intensity and duration in patients undergoing rescue therapy. While no significant outcome difference was detected in the first group between naive and NRTI-experienced patients, among the salvage subjects the change of one or more NRTIs seemed to significantly improve virological and immunological outcome. Viral genotyping detected at least the K103N mutation in 41% of the 78 evaluable patients, despite lack of exposure to efavirenz and related compounds. Salvage patients had a significantly greater frequency of non-nucleoside RTI (NNRTI) resistance compared with the first-line group (P < 0.0001), in proportion to the extent of mutations affecting other drug classes (P < 0.0001).

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Throughout the 96 weeks of the SPRING-1 study, DTG demonstrated sustained efficacy and favorable safety/tolerability in treatment-naive individuals with HIV-1.

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We identified 120 IDUs receiving HAART and methadone within a directly observed therapy (DOT) program. Follow-up was according to clinical standards, with changes in methadone dose being made as required to achieve clinical stabilization within the first 3 months of HAART.

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Sixteen per cent of patients were classified as having virological failure (47 on TDF and 49 on d4T; P = 0.91). Patients with non-B HIV-1 subtypes or baseline nucleoside reverse transcriptase inhibitor (NRTI)-associated mutations responded similarly to the overall population. Resistance to EFV (K103N and others) or 3TC (M184V) developed most frequently (8.3% and 5.8%, respectively) and similarly in the two arms. In the d4T arm, a variety of NRTI mutations developed: K65R (n = 2), L74V (n = 2), V75M (n = 1), and T69A + Y115H (n = 1). K65R developed in eight TDF patients (2.7%); in seven of these eight patients, within 48 weeks. All eight patients began new regimens with a protease inhibitor (PI) and NRTIs, including two patients who remained on TDF; five of the eight patients achieved HIV RNA <50 copies/mL in second-line therapy with the remaining patients having no follow-up or being nonadherent.

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VF rates were observed in one-third of long-term treated Thai children on first-line HAART. Age 3-9 years at HAART initiation was associated with less VF compared with those younger or older, whereas children who used nevirapine had higher VF.

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Concomitant use of combination antiretroviral regimen (cART) and cancer chemotherapy is difficult due to complex interactions and increased toxicity. Raltegravir could be an adequate option through its favourable drug-drug interaction profile.

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Plasma concentrations of efavirenz and rifampicin were quantified by using validated high performance liquid chromatography assays, and pharmacokinetic parameter values were determined by noncompartmental methods. The differences between pharmacokinetic parameters on days 7 and 14 were used to assess interactions.

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Between 2009 and 2011, we recruited adults attending ART centers 10-14 months (the M12 group) or 22-26 months (M24 group) after initiating ART. Demographic and clinical data were collected on site, and viral load was measured. Samples with a viral load of ≥ 1000 copies/mL, considered as the failure threshold, were genotyped for drug resistance assessment.

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This method allows fast and simultaneous quantification of all commercially available PIs and NNRTIs for therapeutic drug monitoring.

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A total of 222 adults were successfully genotyped for HIV drug resistance between December 2010 and March 2012. The most common regimens at time of genotype were stavudine, lamivudine and efavirenz (51%); and stavudine, lamivudine and nevirapine (24%). Median duration of ART was 42 months (interquartile range (IQR) 32-53) and median duration of antiretroviral failure was 27 months (IQR 17-40). One hundred and ninety one (86%) had at least one drug resistance mutation. For 34 individuals (15%), the GSS for the standard second-line regimen was <2, suggesting a significantly compromised regimen. In univariate analysis, individuals with a prior nucleoside reverse-transcriptase inhibitor (NRTI) substitution were more likely to have a GSS <2 than those on the same NRTIs throughout (odds ratio (OR) 5.70, 95% confidence interval (CI) 2.60-12.49).

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This was a randomized open-label 96-week prospective pilot study evaluating four first-line regimens: tenofovir/emtricitabine/nevirapine (group 1), tenofovir/lopinavir/ritonavir (group 2), tenofovir/emtricitabine/zidovudine (group 3) and tenofovir/emtricitabine/efavirenz (group 4) in antiretroviral-naive, HIV-1-infected patients in Senegal and Cameroon. The primary end point was defined as an HIV-1 RNA viral load <50 copies/ml (study detection limit) at week 16 in ≥50% of patients using intention-to-treat analysis.

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Five multiplex assays were developed, comprising the following 15 SNPs: -82T --> C (*22); 86G --> C (R29T, *17); 136A --> G (M46V, *11); 296G --> A (G99E, *12); 415A --> G (K139E, *8, *13); 419G --> A (R140Q, *14); 516G --> T (Q172H, *6, *7, *9, *13, *19, *20), 547G --> A (V183I); 769G --> A (D257N); 785A --> G (K262R, *4, *6, *7, *13, *16, *19, *20); 983T-->C (I328T, *16, *18); 1006C --> T (R336C, *19); 1172T --> A (I391N, *15); 1282C --> A (P428T, *21); 1459C --> T (R487C, *5, *7). In 9 DNA samples showing discrepant genotypes, correctness of the MALDI-TOF MS result was confirmed by direct sequencing.

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TaqMan® low density arrays and LC-MS/MS based targeted proteomics were used to evaluate transporter expression in Caco-2 cells in comparison with jejunal tissue, in culture-time dependence studies and after incubation with different known inducers of drug metabolism and transport. Additionally, studies on ABCB1 function were performed using Transwell® assays with [(3) H]-digoxin and [(3) H]-talinolol as substrates after incubation with the prototypical inducers rifampicin, St John's wort, carbamazepine and efavirenz.

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This randomized, double-blind study involved three antiretroviral regimens for the initial treatment of subjects infected with HIV-1: zidovudine-lamivudine-abacavir, zidovudine-lamivudine plus efavirenz, and zidovudine-lamivudine-abacavir plus efavirenz.

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Random urine samples from 30 patients on EFV therapy were analysed for THC metabolites by two near-testing devices (THC One Step Marijuana and Rapid Response(®) Drugs Atarax 10 Mg Tabletas Precio of Abuse Test Strips) and two automated immunoassays (Roche Diagnostics Cannabinoids II and Beckman Coulter SYNCHRON(®) Systems THC2). THC confirmatory testing was performed by gas chromatography-mass spectrometry (GC-MS).

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To determine whether antiretroviral (ARV) medications can be detected in meconium from second or third Zofran Recommended Dosage Iv trimester, labor and delivery (L&D), or postnatal exposures.

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Rilpivirine (RPV) is a new once-daily, non-nucleoside, reverse transcriptase inhibitor (NNRTI). In treatment-naïve patients, RPV has shown non-inferior antiviral activity to efavirenz but data in treatment-experienced patients are more limited. We assessed the efficacy and safety of RPV in treatment-experienced patients switching Paracetamol Dosage By Weight Adults to a RPV-based regimen.

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Prolonged Geodon 60 Mg Efectos Secundarios QT intervals were not observed in opioid-dependent subjects receiving buprenorphine/naloxone alone. QT interval increases were observed with buprenorphine/naloxone in combination with either delavirdine or ritonavir, which inhibit CYP3A4.

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The use of traditional/complementary/alternate medicines (TCAMs) in HIV/AIDS patients who reside in Southern Africa is quite common. Those who use TCAMs in addition to antiretroviral (ARV) treatment may be at risk of experiencing clinically significant pharmacokinetic (PK) interactions, particularly between the TCAMs and the protease inhibitors (PIs) and non-nucleoside reverse transcriptase inhibitors (NNRTIs). Mechanisms of PK interactions include alterations to the normal functioning of drug efflux transporters, such as P-gp and/or CYP isoenzymes, such a CYP3A4 that mediate the absorption and elimination of drugs in the small intestine and liver. Specific mechanisms include inhibition and activation of these proteins and induction via the pregnane X receptor (PXR). Several clinical studies and case reports involving ARV-herb PK interactions have been reported. St John's Wort, Garlic and Cat's Claw exhibited potentially significant interactions, each with a PI or NNRTI. The potential for these herbs to induce PK interactions with drugs was first identified in reports of in Buy Cialis Professional 20 Mg vitro studies. Other in vitro studies have shown that several African traditional medicinal (ATM) plants and extracts may also demonstrate PK interactions with ARVs, through effects on CYP3A4, P-gp and PXR. The most complex effects were exhibited by Hypoxis hemerocallidea, Sutherlandia frutescens, Cyphostemma hildebrandtii, Acacia nilotica, Agauria salicifolia and Elaeodendron buchananii. Despite a high incidence of HIV/AIDs in the African region, only one clinical study, between efavirenz and Hypoxis hemerocallidea has been conducted. However, several issues/concerns still remain to be addressed and thus more studies on ATMs are warranted in order for more meaningful data to be generated and the true potential for such interactions to be determined.

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Genetic factors have been associated with efavirenz (EFV) plasma concentrations in different populations. In this study, we investigated the effects of CYP2B6 516G>T (rs3745274), CYP2B6 c.485-18C>T (rs4803419), CAR c.540C>T (rs2307424), CAR Cefixime Alcohol c.152-1089T>C (rs3003596), and smoking status in a cohort of Serbian patients with HIV.

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Pretreatment characteristics were median age 38 years, 82% male, 40% white, 10% history of IDU (HxIDU), median CD4+ T-lymphocyte 227 cells/μl and 33% HIV RNA more than 100 ,000 copies/ml. In a multivariable model, factors associated with year 1 EFV success were race [white odds ratio (OR) 1.5; P <  Levitra 80 Mg 0.001; Hispanic OR 1.5; P = 0.003 vs. black], no pretreatment sign/symptom grade 3 or higher (OR 1.7; P = 0.008) and no HxIDU (OR 1.7; P = 0.001). Predictors of EFV success at years 2-5 were no HxIDU (years 2-5; ORs 1.9-2.2); self-reported complete (4 days prior to study visit) adherence during year 1 (years 2-4; ORs 1.6-1.9); fewer missed visits during year 1 (years 2, 4, 5; ORs 0.92-0.98/1% increase); HIV RNA less than 50 copies/ml at year 1 (years 2, 3; ORs 1.9-2.2); and older age (>50 vs. ≤30 years) (years 2-4: ORs 2.3-3.7).

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Atazanavir is the first once-daily protease inhibitor for the treatment of human immunodeficiency virus type 1 infection and should be used only in combination therapy, as part of a highly active antiretroviral therapy (HAART) regimen. In addition to being the most potent protease inhibitor in vitro, atazanavir has a distinct cross-resistance profile that does not confer resistance to other protease Glucophage Maximum Dose inhibitors. However, resistance to other protease inhibitors often confers clinically relevant resistance to atazanavir. Currently, atazanavir is not a preferred protease inhibitor for initial HAART regimens. In treatment-naive patients, atazanavir can be given as 400 mg/day. However, atazanavir should be pharmacologically boosted with ritonavir in treatment-experienced patients or when coadministered with either tenofovir or efavirenz. Patients who receive atazanavir experience similar rates of adverse events compared with patients receiving comparator regimens. An exception is an increased risk of asymptomatic hyperbilirubinemia, which is due to competitive inhibition of uridine diphosphate-glucuronosyltransferase 1A1. Although hyperbilirubinemia is a common adverse drug reaction of atazanavir therapy (22-47%), fewer than 2% of patients discontinue atazanavir therapy because of this adverse effect. Common adverse effects reported with atazanavir include infection, nausea, vomiting, diarrhea, abdominal pain, headache, peripheral neuropathy, and rash. Of significance, fewer abnormalities have been observed in plasma lipid profiles in patients treated with atazanavir compared with other protease inhibitor-containing regimens. As with other protease inhibitors, atazanavir is also a substrate and moderate inhibitor of the cytochrome P450 (CYP) system, in particular CYP3A4 and CYP2C9. Clinically significant drug interactions include (but are not limited to) antacids, proton pump inhibitors, histamine type 2 receptor antagonists, tenofovir, diltiazem, irinotecan, simvastatin, lovastatin, St. John's wort, and warfarin. We conclude that atazanavir is a distinctively characteristic protease inhibitor owing to its in vitro potency, once-daily dosing, distinct initial resistance pattern, and infrequent association with metabolic abnormalities.

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Antiretroviral-naive individuals commencing efavirenz or nevirapine with dual-nucleoside analogue backbones were identified from a prospective database. Virological Azulfidine 500 Mg Medication success was defined as HIV viral load <500 copies per milliliter. Treatment failure was defined as a switch or discontinuation of NNRTI or documented virological failure (2 measurements with viral load >500 copies/mL).

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Using this definition, observed differences between centers included the use of stavudine, abacavir-, and/or efavirenz-based regimens and use of online expert Mestinon Overdose Side Effects advice.

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We did this retrospective cohort study of HIV-positive women aged 15-45 years enrolled in 19 HIV care facilities supported by Family AIDS Care and Education Services in western Kenya between Jan 1, 2011, and Dec 31, 2013. Our primary outcome was incident pregnancy diagnosed clinically. The primary exposure was a combination of contraceptive method and efavirenz-based or nevirapine-based ART regimen. We used Poisson models, adjusting for repeated measures, and demographic, behavioural, and clinical factors, to compare pregnancy rates among women receiving different contraceptive and ART combinations.

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Dyslipidaemia has emerged as an important issue in HIV-infected individuals receiving antiretroviral therapy. This study demonstrates that age at start of therapy, baseline cholesterol level, stavudine use and PI use are all associated with increased risk of hypercholesterolemia on initial therapy. Both NRTI and NNRTI/PI choice influence risk of hypercholesterolaemia.