PACKAGE LABEL.PRINCIPAL DISPLAY PANEL

PRINCIPAL DISPLAY PANEL - 25 mg Tablet Bottle Label

NDC 61958-2301-1

30 tablets

Vemlidy®

(tenofovir alafenamide)

tablets, 25 mg

Note to pharmacist:

Do not cover ALERT box with pharmacy label.

ALERT: Find out about medicines that

should NOT be taken with Vemlidy

RECENT MAJOR CHANGES SECTION

RECENT MAJOR CHANGES

Indications and Usage (1)	03/2024
Dosage and Administration: Recommended Dosage in Adults and Pediatric Patients 6 Years of Age and Older and Weighing at Least 25 kg (2.2)	03/2024

DESCRIPTION SECTION

11 DESCRIPTION

VEMLIDY is a tablet containing tenofovir alafenamide for oral administration. Tenofovir alafenamide, a hepatitis B virus (HBV) nucleoside analog reverse transcriptase inhibitor, is converted in vivo to tenofovir, an acyclic nucleoside phosphonate (nucleotide) analog of adenosine 5′-monophosphate.

Each tablet contains 25 mg of tenofovir alafenamide (equivalent to 28 mg of tenofovir alafenamide fumarate). The tablets include the following inactive ingredients: croscarmellose sodium, lactose monohydrate, magnesium stearate, and microcrystalline cellulose. The tablets are film coated with a coating material containing: iron oxide yellow, polyethylene glycol, polyvinyl alcohol, talc, and titanium dioxide.

The chemical name of tenofovir alafenamide fumarate drug substance is L-alanine, N-[(S)-[[(1R)-2-(6-amino-9H-purin-9-yl)-1-methylethoxy]methyl]phenoxyphosphinyl]-, 1-methylethyl ester, (2E)-2-butenedioate (2:1).

It has an empirical formula of C21H29O5N6P∙½(C4H4O4) and a formula weight of 534.50. It has the following structural formula:

Chemical Structure

Tenofovir alafenamide fumarate is a white to off-white or tan powder with a solubility of 4.7 mg per mL in water at 20 °C.

CLINICAL PHARMACOLOGY SECTION

12 CLINICAL PHARMACOLOGY

12.1 Mechanism of Action

Tenofovir alafenamide is an antiviral drug against the hepatitis B virus [see Microbiology (12.4)].

12.2 Pharmacodynamics

Cardiac Electrophysiology

In a thorough QT/QTc study in 48 healthy subjects, tenofovir alafenamide at the recommended dose or at a dose 5 times the recommended dose did not affect the QT/QTc interval and did not prolong the PR interval.

12.3 Pharmacokinetics

The pharmacokinetic properties of VEMLIDY are provided in Table 5. The multiple dose PK parameters of tenofovir alafenamide and its metabolite tenofovir are provided in Table 6.

Table 5 Pharmacokinetic Properties of VEMLIDY

	Tenofovir Alafenamide
CES1 = carboxylesterase 1; PBMCs = peripheral blood mononuclear cells.
Values refer to geometric mean ratio in AUClast [fed/fasted] and (90% confidence interval). High fat meal = ~800 kcal, 50% fat. † In vivo, TAF is hydrolyzed within cells to form tenofovir (major metabolite), which is phosphorylated to the active metabolite, tenofovir diphosphate. In vitro studies have shown that TAF is metabolized to tenofovir by CES1 in hepatocytes, and by cathepsin A in PBMCs and macrophages. ‡ t1/2 values refer to median terminal plasma half-life. § Dosing in mass balance study: TAF 25 mg (single dose administration of [14C] TAF).
Absorption
Tmax (h)	0.48
Effect of high fat meal (relative to fasting): AUClast Ratio*	1.65 (1.51, 1.81)
Distribution
% Bound to human plasma proteins	80%
Source of protein binding data	Ex vivo
Blood-to-plasma ratio	1.0
Metabolism
Metabolism†	CES1 (hepatocytes) Cathepsin A (PBMCs) CYP3A (minimal)
Elimination
Major route of elimination	Metabolism (>80% of oral dose)
t1/2 (h)‡	0.51
% Of dose excreted in urine§	<1
% Of dose excreted in feces§	31.7

Table 6 Multiple Dose PK Parameters of Tenofovir Alafenamide and its Metabolite Tenofovir Following Oral Administration in Adults with Chronic Hepatitis B

Parameter Mean (CV%)	Tenofovir Alafenamide*	Tenofovir*
CV = coefficient of variation; NA = not applicable
From Intensive PK analyses in Trial 108 and Trial 110; N = 8.
Cmax (mcg per mL)	0.27 (63.3)	0.03 (24.6)
AUCtau (mcg∙hour per mL)	0.27 (47.8)	0.40 (35.2)
Ctrough (mcg per mL)	NA	0.01 (39.6)

Specific Populations

Geriatric Patients, Race, and Gender

Limited data in subjects aged 65 years and over suggest a lack of clinically relevant differences in tenofovir alafenamide or tenofovir pharmacokinetics. No clinically relevant differences in tenofovir alafenamide or tenofovir pharmacokinetics due to race or gender have been identified [see Use in Specific Populations (8.5)].

Pediatric Patients

Steady-state pharmacokinetics of tenofovir alafenamide and its metabolite tenofovir were evaluated in HBV-infected pediatric subjects aged 6 to less than 18 years (Table 7).

Table 7 Multiple Dose PK Parameters of Tenofovir Alafenamide and Tenofovir Following Oral Administration of VEMLIDY 25 mg in HBV-Infected Pediatric Subjects Aged 6 to less than 18 Years

Age Group	Parameter Mean (CV%)	Tenofovir Alafenamide*	Tenofovir†
CV = coefficient of variation; NA = not applicable
From Intensive PK analyses in Trial 1092: Cohort 1, N=13 except N=11 for AUCtau; Cohort 2, Group 1, N=5. † From Intensive PK analyses in Trial 1092: Cohort 1, N=13; Cohort 2, Group 1, N=5.
12 to <18 Years weighing ≥35 kg	Cmax (mcg per mL)	0.188 (45.0)	0.015 (23.5)
AUCtau (mcg∙hour per mL)	0.254 (36.4)	0.244 (28.3)
Ctrough (mcg per mL)	NA	0.0079 (35.0)
6 to <12 Years weighing ≥25 kg	Cmax (mcg per mL)	0.388 (96.9)	0.017 (19.6)
AUCtau (mcg∙hour per mL)	0.313 (64.8)	0.272 (17.5)
Ctrough (mcg per mL)	NA	0.0089 (10.2)

Patients with Renal Impairment

In a Phase 1, open-label study, tenofovir alafenamide and tenofovir systemic exposures (AUCinf) were evaluated in subjects with severe renal impairment and in subjects with normal renal function (Table 8). In an open-label trial of elvitegravir/cobicistat/emtricitabine/tenofovir alafenamide 150/150/200/10 mg, tenofovir alafenamide and tenofovir AUC were evaluated in a subset of virologically suppressed HIV-1 infected subjects with ESRD receiving chronic hemodialysis (Table 8). In a Phase 2, open-label trial, tenofovir alafenamide and tenofovir AUC were evaluated in a subset of virologically suppressed HBV- infected subjects with ESRD receiving chronic hemodialysis (Table 8) [see Use in Specific Populations (8.6)]. The pharmacokinetics of tenofovir alafenamide were similar among subjects with normal renal function, subjects with severe renal impairment, and subjects with ESRD receiving chronic hemodialysis. Relative to those with normal renal function, increased tenofovir exposures were observed in subjects with severe renal impairment and subjects with ESRD receiving chronic hemodialysis. Within the chronic hemodialysis population, increased tenofovir exposures were observed in subjects with HBV relative to those with HIV.

Table 8 Pharmacokinetics of Tenofovir Alafenamide and its Metabolite Tenofovir in Subjects with Renal Impairment as Compared to Subjects with Normal Renal Function

Estimated Creatinine Clearance* Mean (CV%)	≥90 mL per minute 25 mg TAF (N=13)†	15–29 mL per minute 25 mg TAF (N=14)†	<15 mL per minute 25 mg TAF‡ (N=5)	<15 mL per minute 10 mg TAF§ (N=12)
CV = coefficient of variation
By Cockcroft-Gault method. † PK assessed on a single dose of TAF 25 mg in subjects with normal renal function and in subjects with severe renal impairment. ‡ PK assessed on the day prior to hemodialysis of TAF 25 mg. These subjects from Trial 4035 had a median baseline eGFR by Cockcroft-Gault of 7.2 mL/min (range, 4.8 to 12.0). § Exposures from TAF 25 mg = exposures from TAF 10 mg as part of elvitegravir/cobicistat/emtricitabine/tenofovir alafenamide. PK assessed on the day prior to hemodialysis following 3 consecutive daily doses of elvitegravir/cobicistat/emtricitabine/tenofovir alafenamide. These subjects from Trial 1825 had a median baseline eGFR by Cockcroft-Gault of 10.2 mL/min (range, 6.8 to 19.2) . ¶ AUCinf. `AUClast.` Þ `AUCtau.` ß `N=10.`
Tenofovir alafenamide
AUC (mcg∙hour per mL)	0.27 (49.2)¶	0.51 (47.3)¶	0.30 (26.7)#	0.23 (53.2)#
Cmax (mcg per mL)	0.20 (62.1)	0.36 (65.7)	0.23 (48.4)	0.25 (75.4)
Tenofovir
AUC (mcg∙hour per mL)	0.34 (27.2)¶	2.07 (47.1)¶	18.8 (30.4)Þ	8.72 (39.4)Þ,ß
Cmax (mcg per mL)	0.01 (36.5)	0.03 (32.4)	0.89 (26.4)	0.44 (40.9)
C24h (mcg per mL)	0.004 (25.6)	0.02 (41.9)	0.89 (26.4)	0.26 (73.2)ß

Patients with Hepatic Impairment

Tenofovir alafenamide and tenofovir pharmacokinetics are similar in subjects with mild (Child-Pugh Class A) hepatic impairment and in subjects with normal hepatic function.

HIV and/or Hepatitis C Virus Coinfection

The pharmacokinetics of tenofovir alafenamide have not been fully evaluated in subjects coinfected with HIV and/or hepatitis C virus.

Drug Interaction Studies

[see Drug Interactions (7)]

The effects of coadministered drugs on the exposure of tenofovir alafenamide are shown in Table 9. The effects of tenofovir alafenamide on the exposure of coadministered drugs are shown in Table 10 [For information regarding clinical recommendations, see Drug Interactions (7)]. Information regarding potential drug-drug interactions with HIV antiretrovirals is not provided (see the prescribing information for emtricitabine/tenofovir alafenamide for interactions with HIV antiretrovirals).

Table 9 Drug Interactions: Changes in Pharmacokinetic Parameters for Tenofovir Alafenamide in the Presence of the Coadministered Drug*

Coadministered Drug	Dose of Coadministered Drug (mg)	Tenofovir Alafenamide (mg)	N	Geometric Mean Ratio of TAF Pharmacokinetic Parameters (90% CI)†; No effect = 1.00
Cmax	AUC	Cmin
NC = not calculated
All interaction studies conducted in healthy subjects. † All no effect boundaries are 70%–143%. ‡ Study conducted with emtricitabine/tenofovir alafenamide. § A representative inhibitor of P-glycoprotein. ¶ Study conducted with emtricitabine/rilpivirine/tenofovir alafenamide. `Study conducted with elvitegravir/cobicistat/emtricitabine/tenofovir alafenamide.` Þ `Study conducted with additional voxilaprevir 100 mg to achieve voxilaprevir exposures expected in HCV-infected patients.`
Carbamazepine	300 twice daily	25 once daily‡	26	0.43 (0.36, 0.51)	0.45 (0.40, 0.51)	NC
Cobicistat§	150 once daily	8 once daily	12	2.83 (2.20, 3.65)	2.65 (2.29, 3.07)	NC
Ledipasvir/ Sofosbuvir	90/400 once daily	25 once daily¶	42	1.03 (0.94, 1.14)	1.32 (1.25, 1.40)	NC
Sertraline	50 single dose	10 once daily#	19	1.00 (0.86, 1.16)	0.96 (0.89, 1.03)	NC
Sofosbuvir/ Velpatasvir/ Voxilaprevir	400/100/100+100 voxilaprevirÞ once daily	25 once daily¶	30	1.32 (1.17, 1.48)	1.52 (1.43, 1.61)	NC

Table 10 Drug Interactions: Changes in Pharmacokinetic Parameters for Coadministered Drug in the Presence of Tenofovir Alafenamide*

Coadministered Drug	Dose of Coadministered Drug (mg)	Tenofovir Alafenamide (mg)	N	Geometric Mean Ratio of Coadministered Drug Pharmacokinetic Parameters (90% CI)†; No effect = 1.00
Cmax	AUC	Cmin
NC = not calculated
All interaction studies conducted in healthy subjects. † All no effect boundaries are 70%–143%. ‡ Study conducted with emtricitabine/rilpivirine/tenofovir alafenamide. § The predominant circulating nucleoside metabolite of sofosbuvir. ¶ A sensitive CYP3A4 substrate. `Study conducted with emtricitabine/tenofovir alafenamide.` Þ `Study conducted with elvitegravir/cobicistat/emtricitabine/tenofovir alafenamide.` ß `Study conducted with emtricitabine/rilpivirine/tenofovir alafenamide.` à `Study conducted with additional voxilaprevir 100 mg to achieve voxilaprevir exposures expected in HCV-infected patients.`
Ledipasvir	90 ledipasvir / 400 sofosbuvir once daily	25 once daily‡	41	1.01 (0.97, 1.05)	1.02 (0.97, 1.06)	1.02 (0.98, 1.07)
Sofosbuvir	0.96 (0.89, 1.04)	1.05 (1.01, 1.09)	NC
GS-331007§	1.08 (1.05, 1.11)	1.08 (1.06, 1.10)	1.10 (1.07, 1.12)
Midazolam¶	2.5 single dose orally	25 once daily	18	1.02 (0.92, 1.13)	1.13 (1.04, 1.23)	NC
1 single dose IV	0.99 (0.89, 1.11)	1.08 (1.04, 1.14)	NC
Norelgestromin	norgestimate 0.180/0.215/0.250 once daily / ethinyl estradiol 0.025 once daily	25 once daily#	29	1.17 (1.07, 1.26)	1.12 (1.07, 1.17)	1.16 (1.08, 1.24)
Norgestrel	1.10 (1.02, 1.18)	1.09 (1.01, 1.18)	1.11 (1.03, 1.20)
Ethinyl estradiol	1.22 (1.15, 1.29)	1.11 (1.07, 1.16)	1.02 (0.93, 1.12)
Sertraline	50 single dose	10 once dailyÞ	19	1.14 (0.94, 1.38)	0.93 (0.77, 1.13)	NC
Sofosbuvir	400 once daily	25 once dailyß	30	0.95 (0.86, 1.05)	1.01 (0.97, 1.06)	NC
GS-331007§	1.02 (0.98, 1.06)	1.04 (1.01, 1.06)	NC
Velpatasvir	100 once daily	1.05 (0.96, 1.16)	1.01 (0.94, 1.07)	1.01 (0.95, 1.09)
Voxilaprevir	100+100à once daily	0.96 (0.84, 1.11)	0.94 (0.84, 1.05)	1.02 (0.92, 1.12)

12.4 Microbiology

Mechanism of Action

Tenofovir alafenamide is a phosphonamidate prodrug of tenofovir (2'-deoxyadenosine monophosphate analog). Tenofovir alafenamide as a lipophilic cell-permeant compound enters primary hepatocytes by passive diffusion and by the hepatic uptake transporters OATP1B1 and OATP1B3. Tenofovir alafenamide is then converted to tenofovir through hydrolysis primarily by carboxylesterase 1 (CES1) in primary hepatocytes. Intracellular tenofovir is subsequently phosphorylated by cellular kinases to the pharmacologically active metabolite tenofovir diphosphate. Tenofovir diphosphate inhibits HBV replication through incorporation into viral DNA by the HBV reverse transcriptase, which results in DNA chain-termination.

Tenofovir diphosphate is a weak inhibitor of mammalian DNA polymerases that include mitochondrial DNA polymerase γ and there is no evidence of toxicity to mitochondria in cell culture.

Antiviral Activity in Cell Culture

The antiviral activity of tenofovir alafenamide was assessed in a transient transfection assay using HepG2 cells against a panel of HBV clinical isolates representing genotypes A-H. The EC50 (50% effective concentration) values for tenofovir alafenamide ranged from 34.7 to 134.4 nM, with an overall mean EC50 value of 86.6 nM. The CC50 (50% cytotoxicity concentration) values in HepG2 cells were greater than 44,400 nM. In cell culture combination antiviral activity studies of tenofovir with the HBV nucleoside reverse transcriptase inhibitors entecavir, lamivudine, and telbivudine, no antagonistic activity was observed.

Resistance in Clinical Trials

Genotypic resistance analysis was performed on paired baseline and on- treatment HBV isolates for subjects who either experienced virologic breakthrough (2 consecutive visits with HBV DNA greater than or equal to 69 IU/mL [400 copies/mL] after having been less than 69 IU/mL, or 1.0-log10 or greater increase in HBV DNA from nadir) through Week 48, or had HBV DNA greater than or equal to 69 IU/mL at early discontinuation at or after Week 24.

In a pooled analysis of treatment-naïve and treatment-experienced subjects receiving VEMLIDY in Trials 108 and 110 [see Clinical Studies (14.2)], treatment-emergent amino acid substitutions in the HBV reverse transcriptase domain, all occurring at polymorphic positions, were observed in some HBV isolates evaluated (5/20); however, no specific substitutions occurred at a sufficient frequency to be associated with resistance to VEMLIDY.

In virologically suppressed subjects receiving VEMLIDY in Trial 4018 [see Clinical Studies (14.3)], no subjects qualified for resistance analysis through 48 weeks of VEMLIDY treatment.

In pediatric Trial 1092, 17/70 subjects in Cohort 1 (aged 12 to less than 18 years) and 7/18 subjects in Cohort 2, Group 1 (aged 6 to less than 12 years) receiving VEMLIDY qualified for resistance analysis at Week 96. Results were obtained from 19/24 qualified subjects. No HBV amino acid substitutions known to be associated with resistance to tenofovir alafenamide were detected through 96 weeks of treatment [see Clinical Studies (14.5)].

Cross-Resistance

The antiviral activity of tenofovir alafenamide was evaluated against a panel of isolates containing substitutions associated with HBV nucleoside reverse transcriptase inhibitor resistance in a transient transfection assay using HepG2 cells. HBV isolates expressing the lamivudine resistance-associated substitutions rtM204V/I (±rtL180M±rtV173L) and expressing the entecavir resistance-associated substitutions rtT184G, rtS202G, or rtM250V in the presence of rtL180M and rtM204V showed less than 2-fold reduced susceptibility (within the inter-assay variability) to tenofovir alafenamide. HBV isolates expressing the rtA181T, rtA181V, or rtN236T single substitutions associated with resistance to adefovir also had less than 2-fold changes in EC50 values; however, the HBV isolate expressing the rtA181V plus rtN236T double substitutions exhibited reduced susceptibility (3.7-fold) to tenofovir alafenamide. The clinical relevance of these substitutions is not known.

INDICATIONS & USAGE SECTION

Highlight: VEMLIDY is a hepatitis B virus (HBV) nucleoside analog reverse transcriptase inhibitor and is indicated for the treatment of chronic hepatitis B virus infection in adults and pediatric patients 6 years of age and older and weighing at least 25 kg with compensated liver disease. (1)

1 INDICATIONS AND USAGE

VEMLIDY is indicated for the treatment of chronic hepatitis B virus (HBV) infection in adults and pediatric patients 6 years of age and older and weighing at least 25 kg with compensated liver disease [see Clinical Studies (14)].

DOSAGE FORMS & STRENGTHS SECTION

Highlight: Tablets: 25 mg of tenofovir alafenamide. (3)

3 DOSAGE FORMS AND STRENGTHS

Tablets: 25 mg of tenofovir alafenamide (equivalent to 28 mg of tenofovir alafenamide fumarate) — yellow, round, film-coated tablets, debossed with "GSI" on one side of the tablet and "25" on the other side.

CONTRAINDICATIONS SECTION

Highlight: None. (4)

4 CONTRAINDICATIONS

None.

BOXED WARNING SECTION

WARNING: POSTTREATMENT SEVERE ACUTE EXACERBATION OF HEPATITIS B

WARNINGS AND PRECAUTIONS SECTION

Highlight: * HBV and HIV-1 coinfection: VEMLIDY alone is not recommended for the treatment of HIV-1 infection. HIV-1 resistance may develop in these patients. (5.2)

New onset or worsening renal impairment: Prior to or when initiating VEMLIDY, and during treatment on a clinically appropriate schedule, assess serum creatinine, estimated creatinine clearance, urine glucose, and urine protein in all patients. Also assess serum phosphorus in patients with chronic kidney disease. (5.3)
Lactic acidosis/severe hepatomegaly with steatosis: Discontinue treatment in patients who develop symptoms or laboratory findings suggestive of lactic acidosis or pronounced hepatotoxicity. (5.4)

5 WARNINGS AND PRECAUTIONS

5.1 Severe Acute Exacerbation of Hepatitis B after Discontinuation of

Treatment

Discontinuation of anti-hepatitis B therapy, including VEMLIDY, may result in severe acute exacerbations of hepatitis B. Patients who discontinue VEMLIDY should be closely monitored with both clinical and laboratory follow-up for at least several months after stopping treatment. If appropriate, resumption of anti-hepatitis B therapy may be warranted.

5.2 Risk of Development of HIV-1 Resistance in Patients Coinfected with HBV

and HIV-1

Due to the risk of development of HIV-1 resistance, VEMLIDY alone is not recommended for the treatment of HIV-1 infection. The safety and efficacy of VEMLIDY have not been established in patients coinfected with HBV and HIV-1. HIV antibody testing should be offered to all HBV-infected patients before initiating therapy with VEMLIDY, and, if positive, an appropriate antiretroviral combination regimen that is recommended for patients coinfected with HIV-1 should be used.

5.3 New Onset or Worsening Renal Impairment

Postmarketing cases of renal impairment, including acute renal failure, proximal renal tubulopathy (PRT), and Fanconi syndrome have been reported with TAF-containing products; while most of these cases were characterized by potential confounders that may have contributed to the reported renal events, it is also possible these factors may have predisposed patients to tenofovir- related adverse events [see Adverse Reactions (6.2)].

Patients taking tenofovir prodrugs who have impaired renal function and those taking nephrotoxic agents, including non-steroidal anti-inflammatory drugs, are at increased risk of developing renal-related adverse reactions [see Drug Interactions (7.2)].

Prior to or when initiating VEMLIDY, and during treatment with VEMLIDY on a clinically appropriate schedule, assess serum creatinine, estimated creatinine clearance, urine glucose, and urine protein in all patients. In patients with chronic kidney disease, also assess serum phosphorus. Discontinue VEMLIDY in patients who develop clinically significant decreases in renal function or evidence of Fanconi syndrome [see Adverse Reactions (6.1) and Use in Specific Populations (8.6)].

5.4 Lactic Acidosis/Severe Hepatomegaly with Steatosis

Lactic acidosis and severe hepatomegaly with steatosis, including fatal cases, have been reported with the use of nucleoside analogs, including tenofovir disoproxil fumarate (TDF), another prodrug of tenofovir, alone or in combination with other antiretrovirals. Treatment with VEMLIDY should be suspended in any patient who develops clinical or laboratory findings suggestive of lactic acidosis or pronounced hepatotoxicity (which may include hepatomegaly and steatosis even in the absence of marked transaminase elevations).

OVERDOSAGE SECTION

10 OVERDOSAGE

If overdose occurs, monitor patient for evidence of toxicity. Treatment of overdosage with VEMLIDY consists of general supportive measures including monitoring of vital signs as well as observation of the clinical status of the patient. Tenofovir is efficiently removed by hemodialysis with an extraction coefficient of approximately 54%.

SPL PATIENT PACKAGE INSERT SECTION

This Patient Information has been approved by the U.S. Food and Drug Administration.

Revised: 03/2024

Patient Information
VEMLIDY® (VEM-lih-dee)
(tenofovir alafenamide)
tablets

What is the most important information I should know about VEMLIDY?
VEMLIDY can cause serious side effects, including:

*Worsening of hepatitis B virus (HBV) infection. Your HBV infection may get worse (flare-up) if you take VEMLIDY and then stop taking it. A "flare-up" is when your HBV infection suddenly returns in a worse way than before. *Do not run out of VEMLIDY. Refill your prescription or talk to your healthcare provider before your VEMLIDY is all gone. *Do not stop taking VEMLIDY without first talking to your healthcare provider. * If you stop taking VEMLIDY, your healthcare provider will need to check your health often and do blood tests regularly for several months to check your liver. Tell your healthcare provider about any new or unusual symptoms you may have after you stop taking VEMLIDY.

For more information about side effects, see the section "What are the possible side effects of VEMLIDY?"

What is VEMLIDY?
VEMLIDY is a prescription medicine used to treat chronic (long-lasting) hepatitis B virus (HBV) in adults and children 6 years of age and older who weigh at least 55 pounds (25 kg) with stable (compensated) liver disease.

VEMLIDY may lower the amount of HBV in your body.
VEMLIDY may improve the condition of your liver.

It is not known if VEMLIDY is safe and effective in children with chronic HBV infection who are under 6 years of age or weigh less than 55 pounds (25 kg).

What should I tell my healthcare provider before taking VEMLIDY?
Before taking VEMLIDY, tell your healthcare provider about all of your medical conditions, including if you:

have HIV-1 infection. Your healthcare provider may test you for HIV-1 infection before you start VEMLIDY. If you have both HBV and HIV-1, and you only take VEMLIDY, the HIV-1 virus may develop resistance and become harder to treat.
have end stage renal disease (ESRD).
are pregnant or plan to become pregnant. It is not known if VEMLIDY will harm your unborn baby. Tell your healthcare provider if you become pregnant during treatment with VEMLIDY.
Pregnancy Exposure Registry: There is a pregnancy registry for women who take antiviral medicines during pregnancy. The purpose of this registry is to collect information about the health of you and your baby. Talk with your healthcare provider about how you can take part in this registry.
are breastfeeding or plan to breastfeed. VEMLIDY may pass into your breastmilk. Talk with your healthcare provider about the best way to feed your baby.

Tell your healthcare provider about all the medicines you take, including prescription and over-the-counter medicines, vitamins, and herbal supplements.
Some medicines may affect how VEMLIDY works.

Keep a list of your medicines and show it to your healthcare provider and pharmacist when you get a new medicine. You can ask your healthcare provider or pharmacist for a list of medicines that interact with VEMLIDY. *Do not start a new medicine without telling your healthcare provider. Your healthcare provider can tell you if it is safe to take VEMLIDY with other medicines.

How should I take VEMLIDY?

Take VEMLIDY exactly as your healthcare provider tells you to take it.
Take VEMLIDY 1 time each day.
Take VEMLIDY with food.
If you are on dialysis, on your dialysis days, take your daily dose of VEMLIDY following dialysis.
Do not change your dose or stop taking VEMLIDY without first talking with your healthcare provider. Stay under a healthcare provider's care when taking VEMLIDY. *Do notmiss a dose of VEMLIDY.
If you take too much VEMLIDY, call your healthcare provider or go to the nearest hospital emergency room right away.
When your VEMLIDY supply starts to run low, get more from your healthcare provider or pharmacy. This is very important because your HBV infection may get worse (flare-up) if you stop taking VEMLIDY.

What are the possible side effects of VEMLIDY?
VEMLIDY may cause serious side effects, including:

*See "What is the most important information I should know about VEMLIDY?" *New or worse kidney problems, including kidney failure. Your healthcare provider should do blood and urine tests to check your kidneys when starting and during treatment with VEMLIDY. Your healthcare provider may tell you to stop taking VEMLIDY if you develop new or worse kidney problems. *Too much lactic acid in your blood (lactic acidosis). Too much lactic acid is a serious but rare medical emergency that can lead to death. Tell your healthcare provider right away if you get these symptoms: weakness or being more tired than usual, unusual muscle pain, being short of breath or fast breathing, stomach pain with nausea and vomiting, cold or blue hands and feet, feel dizzy or lightheaded, or a fast or abnormal heartbeat. *Severe liver problems. In rare cases, severe liver problems can happen that can lead to death. Tell your healthcare provider right away if you get these symptoms: skin or the white part of your eyes turns yellow, dark "tea-colored" urine, light-colored stools, loss of appetite for several days or longer, nausea, or stomach-area pain.

The most common side effect of VEMLIDY is headache. Tell your healthcare provider if you have any side effect that bothers you or that does not go away.
These are not all the possible side effects of VEMLIDY. For more information, ask your healthcare provider or pharmacist.
Call your doctor for medical advice about side effects. You may report side effects to FDA at 1-800-FDA-1088.

How should I store VEMLIDY?

Store VEMLIDY below 86 °F (30 °C).
Keep VEMLIDY in its original container.
Keep the container tightly closed.
VEMLIDY comes in a child-resistant package.

Keep VEMLIDY and all medicines out of reach of children.

General information about the safe and effective use of VEMLIDY.
Medicines are sometimes prescribed for purposes other than those listed in a Patient Information leaflet. Do not use VEMLIDY for a condition for which it was not prescribed. Do not give VEMLIDY to other people, even if they have the same symptoms you have. It may harm them. If you would like more information, talk with your healthcare provider. You can ask your healthcare provider or pharmacist for information about VEMLIDY that is written for health professionals.

What are the ingredients in VEMLIDY?
Active ingredients: tenofovir alafenamide
Inactive ingredients: croscarmellose sodium, lactose monohydrate, magnesium stearate, and microcrystalline cellulose. The tablets are film- coated with a coating material containing: iron oxide yellow, polyethylene glycol, polyvinyl alcohol, talc, and titanium dioxide.
Manufactured and distributed by: Gilead Sciences, Inc. Foster City, CA 94404
VEMLIDY is a registered trademark of Gilead Sciences, Inc., or its related companies. © 2024 Gilead Sciences, Inc. All rights reserved.
208464-GS-009
For more information, call 1-800-445-3235 or go to www.VEMLIDY.com.

HOW SUPPLIED SECTION

16 HOW SUPPLIED/STORAGE AND HANDLING

VEMLIDY tablets containing 25 mg of tenofovir alafenamide are yellow, round, film-coated, debossed with "GSI" on one side and "25" on the other side. Each bottle contains 30 tablets (NDC 61958-2301-1), a silica gel desiccant, polyester coil, and is closed with a child-resistant closure.

Store below 30 °C (86 °F).

Keep container tightly closed.
Dispense only in original container.

SPL UNCLASSIFIED SECTION

Manufactured and distributed by: Gilead Sciences, Inc. Foster City, CA 94404

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VEMLIDY

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