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New antiviral drug Clinical indications Resistance Methods of production Uses Adverse effects Pharmacokinetics drug withdrawal Disabling condition
Lamivudine structure
Chemical Name:
Molecular Formula:
Formula Weight:
MOL File:

Lamivudine Properties

Melting point:
177 °C
D21 -135° (c = 0.38 in methanol)
Boiling point:
475.4±55.0 °C(Predicted)
1.73±0.1 g/cm3(Predicted)
refractive index 
-142 ° (C=1, MeOH)
Flash point:
storage temp. 
water: soluble10mg/mL, clear
white to beige
Water Solubility 
70g/L(temperature not stated)
CAS DataBase Reference
134678-17-4(CAS DataBase Reference)
NCI Dictionary of Cancer Terms
NCI Drug Dictionary
ATC code
EPA Substance Registry System
2(1H)-Pyrimidinone, 4-amino-1-[(2R,5S)-2-(hydroxymethyl)-1,3-oxathiolan-5-yl]- (134678-17-4)
  • Risk and Safety Statements
Signal word  Danger
Hazard statements  H361-H225-H301+H311+H331-H370
Precautionary statements  P280-P210-P260-P301+P310+P330-P308+P311-P403+P233-P201-P308+P313-P281
Risk Statements  63-36/37/38
Safety Statements  26-36
RIDADR  UN1230 - class 3 - PG 2 - Methanol, solution
WGK Germany  3
RTECS  UW7361333
HS Code  29349990

Lamivudine price More Price(55)

Manufacturer Product number Product description CAS number Packaging Price Updated Buy
Sigma-Aldrich L-037 Lamivudine 1.0 mg/mL in methanol, certified reference material 134678-17-4 037-1ml $109 2021-12-16 Buy
Sigma-Aldrich 1356836 Lamivudine United States Pharmacopeia (USP) Reference Standard 134678-17-4 200mg $366 2021-12-16 Buy
TCI Chemical L0217 Lamivudine >98.0%(HPLC)(T) 134678-17-4 100mg $16 2021-12-16 Buy
TCI Chemical L0217 Lamivudine >98.0%(HPLC)(T) 134678-17-4 1g $83 2021-12-16 Buy
Cayman Chemical 18514 Lamivudine ≥98% 134678-17-4 50mg $35 2021-12-16 Buy

Lamivudine Chemical Properties,Uses,Production

New antiviral drug

Lamivudine is the (–) enantiomer of a cytidine analogue with sulfur substituted for the 3'carbon atom in the furanose ring [(–) 2',3'-dideoxy, 3'-thiacytidine]. It has significant activity in vitro against both HIV-1 and HIV-2 as well as HBV. Lamivudine is phosphorylated to the triphosphate metabolite by cellular kinases. The triphosphate derivative is a competitive inhibitor of the viral reverse transcriptase.
Lamivudine Tablets
The oral bioavailability in adults is >80% for doses between 0.25 and 8.0 mg kg1. Peak serum concentrations of 1.5 mg ml 1 are achieved in 1–1.5 h and the plasma T1/2 is approximately 2–4 h. Lamivudine is eliminated by the kidneys unchanged by both glomerular filtration and tubular excretion, and dosages should be adapted to creatinine clearance.

Clinical indications

Lamivudine is effective as monotherapy for the treatment of chronic HBV infection and in combination with other antiretroviral drugs for treatment of HIV infection. It is the first line drug for the treatment of HBeAg and anti- HBe positive disease. Elevated serum ALT levels have been shown to predict a higher likelihood of HBeAg loss in patients with chronic hepatitis B treated with lamivudine. Lamivudine is administered orally at 100 mg day1 in the treatment of HBV infections, though the ideal dose could be higher.


Resistance to lamivudine monotherapy develops within 6 months of therapy. The incidence of lamivudine resistance is 15–20% per year, with 70% patients becoming resistant after 5 years of treatment. It will be curious to know if lamivudine at higher doses will affect the incidence of resistance. Lamivudine resistance to HBV is conferred through HBV strains with mutations in the viral polymerase, within the catalytic domain (C domain), which includes the YMDD motif (e.g., M204V or M204I), and within the B domain (e.g., L180M or V173L). These mutants have a reduced replication capacity compared with the wild type HBV virus. Lamivudine resistance is managed by sequential treatment with either adefovir or entecavir. However, the advantage of sequen- tial treatment compared to de novo combination therapy is questionable.

Methods of production

Select 6-o-sulfo acylation reaction to the compounds (I), then acetylated to obtaine compound (II), the yield was 96.7%. The compound (II) uses acetic acid as solvent, and 3 moL hydrogen bromide/L acid (45%, W/V) reaction, bromination to get compound (III), the yield was 99%. Bromide (III) and 3.3 moI ethyl potassium xanthate, refluxing in acetone, thio and cyclization; then in methanol with ammonia hydrolysis to obtain the compound (IV), the second step yield is 72%. Compounds (IV) is purified by column chromatography, is crystalline solid. Compound (IV) uses 1.4 mol sodium periodate treatment to make 2,3-CIS glycol open; followed by sodium borohydride reduction to aldehydes and shrinkage the keto form to protect the glycol, and obtain compound (V), the yield is 60%. The compound (V) silane to protect the rest of the primary alcohol, and then take off ketal to obtain compound (VI) and yield is 63%.Use lead tetraacetate to oxidize glycol of compounds (VI), and then to use dichromic acid pyridine salt to further oxidation, and obtain compound (VII), the oxidation method does not affect the sulfur. compounds (VII) is oxidized by using lead acetate to obtain compounds (VIII), the yield is 66%[ according to compounds (VI)]. Compounds (VIII) and (IX) are in the dichloroethane,and TMSOTf as a Lewis acid catalyst, condensated to compound (x), the yield is 64%. And the amount of isomers of compounds (x) is half of the compounds (x) and their available silica gel chromatography to isolate. Compounds (x) in ammonia-methanol and acetyl, the yield is 73% ; with Tetrabutylammonium fluoride solution to remove the silylation to obtain lamivudine and yield of 75%.


Lamivudine is a potent nucleoside reverse transcriptase inhibitor. Antiviral. Lamivudine has been used for treatment of chronic hepatitis B.

Adverse effects

Lamivudine has an extremely favorable toxicity profile. This may be partly because lamivudine does not affect mitochondrial DNA synthesis and its poor inhibition of human DNA polymerases. At the highest doses of 20 mg kg-1 day-1, neutropenia is encountered but at a low frequency.


After oral administration of lamivudine, it is well absorbed. And about 0.1 g of adult oral about 1hr reached peak plasma concentration Cmax 1.1-1.5 u g/ml, bioavailability is 80-85%. and at the same time of food taking, the Tmax delayed 0.25-2.5 HR and lower 10-40% of Cmax, but the bioavailability is unchanged. Intravenous administration research results table Ming lamivudine average distribution capacity is 1.3 L/Kg, system average clearance rate of 0.3 L/h/kg, seventy percent by organic cation transport system and renal clearance and elimination half-life is 5-7hr. within the therapeutic dose range and lamivudine pharmacokinetics showed a linear relationship, the plasma protein binding rate is low. In vitro studies have shown that with serum albumin binding rate is <16-36%. It can pass through the blood brain barrier into the cerebrospinal fluid. Mainly the prototype drug excretion by the kidneys, renal excretion accounted for about total removal of 70% or so, only 5-10% is metabolized into Anti sulfur oxide derivatives. For patients with renal insufficiency can affect lamivudine excretion, and for creatinine clearance rate <30mL/ points in patients, does not recommend the use of this product. Liver damage does not affect the metabolism of drugs, due to increased age and decreased renal excretory function in elderly patients, lamivudine metabolism without significant changes, Only in creatinine clear except rate <30mL/ time-sharing, there is influence.

drug withdrawal

Lamivudine is not hepatitis b curative drugs, can only make it better, and easy to rebound after discontinuation of lamivudine treatment. So how long is more appropriate, should according to the therapeutic effect and It differs from man to man. The most accepted standard of withdrawal is: before treatment, HBVDNA positive, HBeAg positive, ALT increased more than 1 times; treatment after HBVDNA seroconversion, HBeAg seroconversion ("big Sanyang" to "small Sanyang"), ALT normalization, maintain the effect of the above 6 months can be stopped. Of course in this standard withdrawal is not only without recurrence, the recurrence rate is low. It is reported that this group of patients discontinued 21 months still maintain curative effect. The recurrence rate of 81%. Asians is slightly higher, but in a year when the recurrence rate is lower than that of 40%. For example not up to this effect and withdrawal, while the majority of cases in a short period of time to recurrence, even some patients because of inappropriate drug withdrawal and lead to illness. So stoping the drug is a great event, I hope the patients in the decision to stop the medicine to go to the hospital to consult an experienced specialist, and not to stop the medicine.

Disabling condition

1.Chronic asymptomatic hepatitis B virus carriers were normal and no symptoms, whatever virus replication index or not (both "big Sanyang" and "small Sanyang"), are not taking lamivudine. But it is understood that at present this part of patients taking this medicine is a common phenomenon, which wasted drugs and money. At present the treatment of hepatitis B virus is not resolved, medical scientists is also exploring, the existing methods are not mature. The important reason of lamivudine in treatment of hepatitis B virus are invalid, someone after taking HBVDNA may drop to 103 copies/ml, once the withdrawal and we immediately rebound. We found that people taking more than half a year after discontinuation of HBVDNA negative, less than 1 months back, and HBeAg cannot be negative. Therefore, can't use this medicine to treat hepatitis B virus, unless the liver puncture biopsy confirmed chronic liver. The application can only be considered when the inflammatory pathological changes.
2. Acute severe hepatitis or acute liver failure are in critical condition, the ferocious. At this time the patient's main contradiction is not virus replication, some patients even without virus replication index, threatening the patient's life is liver failure, according to "the government ease the emergency treatment of the subject", then the most important is supportive therapy, such as the input of fresh plasma, albumin, artificial liver support therapy.
3. Acute exacerbation of chronic hepatitis B, if the transaminase is greater than the upper limit of the normal value of 10 times, there are obvious jaundice, or serum bilirubin than 85.5 mmol/L, temporarily not to take lamivudine and other antiviral drugs, and liver, jaundice and reducing enzyme treatment is given priority to, When remission can apply a small amount. Although lamivudine on immune function has strongly influenced not the same interferon but in the acute exacerbation of hepatitis, prevent damage on the immune system. No use is the best policy.
4. Chronic hepatitis B in pregnancy or pregnancy after HBV infection, do not use this product, the main reasons of the effect of lamivudine on the fetus are yet to be elucidated. As both at home and abroad, There are application reports and relatively safe, but experts in China has not yet reached a consensus, as a precaution, temporarily application is a wise choice.


Lamivudine is a cytidine analog that inhibits the reverse transcriptases of HIV1 (IC50 = 45 nM), HIV2, and hepatitis B. It was one of the first approved nucleoside analog reverse transcriptase inhibitors used to treat viral infections. Following prolonged administration, the efficacy of lamivudine is associated with drug resistance, which may be improved through combination treatments.


Lamivudine is a new generation orally active nucleoside analog launched in the U.S.A. for use in combination with zidovudine (AZT) as a first-line therapy for patients with HIV infection. Lamivudine is rapidly converted to phosphorylated metabolites in the body which act as inhibitors and chain terminators of HIV reverse transcriptase (RT), the enzyme required for the replication of the HIV genome. Lamivudine has similar inhibitory potency to RT as AZT but is 10 times less toxic and is active against AZT-resistant strains of HIV. Combination therapy of lamivudine and AZT produced a large decrease in blood-borne virus with an increase in CD4 cells, an effect that can be sustained for 2 years. Since hepatitis B virus (HBV) also encodes a polymerase with a RT function necessary for the conversion of a RNA replicative intermediate to DNA, clinical efficacy has been reported for lamivudine in treating patients with HBV infection. It was reported that the enantiomer of lamivudine is equipotent against HIV but with considerably higher cytotoxicity.

Chemical Properties

White Crystalline Powder


BioChem Pharma (Canada)


Lamivudine has been used to deplete the Hepatitis B Virus (HBV) covalently closed circular DNA (cccDNA) forms for the preparation of inverse nested PCR.


A reverse transcriptase inhibitor. Antiviral.


ChEBI: A monothioacetal that consists of cytosine having a (2R,5S)-2-(hydroxymethyl)-1,3-oxathiolan-5-yl moiety attached at position 1. An inhibitor of HIV-1 reverse transcriptase.


Lamivudine is a synthetic cytidine analogue used in the treatment of HIV and HBV. Its activation requires phosphorylation by cellular enzymes. Lamivudine triphosphate competitively inhibits HBV DNA polymerase and HIV reverse transcriptase and causes chain termination. It inhibits the activity of mammalian DNA polymerases with a much lower potency.
HIV-1 frequently acquires mutations in reverse transcriptase that result in resistance to lamivudine within 12 weeks of treatment. Mutations in the DNA polymerase of HBV are associated with decreased lamivudine efficacy and have been documented in patients treated with this agent for 6 months or more.

Manufacturing Process

To a solution of potassium t-butoxide (0.11 mol) in 100 ml DMF was added thiobenzoic acid (0.11 mol) and the solution partially evaporated in vacuo, benzene added in two consecutive portions and evaporated in vacuo each time. To the residual DMF solution was added bromoacetaldehyde diethyl acetal (0.1 mol) and the mixture stirred at 120°C for 15 h. After cooling, it was poured onto water (500 ml), the product extracted with ether, the extract washed with aqueous NaHCO3 followed by water, then dried and the solvent removed in vacuo. The residue was distilled in vacuo to give 17.2 g of pure 2- thiobenzoyl acetaldehyde diethyl acetal, boiling point 131-133°C/0.07 mm.
The 2-thiobenzoyl acetaldehyde diethyl acetal (17.2 g) was dissolved in 100 ml THF followed by the addition of 6 g NaOH in 20 ml H2O. The mixture was refluxed under N2 for 15 h, then cooled and diluted with water (200 ml) and the product extracted with ether (3 x 200 ml). The extract was dried, the solvent removed in vacuo and the residue distilled to yield 7.1 g of mercaptoacetaldehyde diethylacetal.
50 g of the 1-benzoyl glycerol in a mixture of 500 ml of CH2Cl2 and 25 ml of H2O was treated portionwise with 80 g of NaIO4 under vigorous stirring at room temperature. After addition, stirring was continued for 2 h after which time 100 g of MgSO4 was added and stirring continued for 30 min. The mixture was filtered, the filtrate evaporated in vacuo and the residue distilled to yield 26 g of pure benzoyloxyacetaldehyde, boiling point 92-94°C/0.25 mm.
The mercaptoacetaldehyde diethylacetal (7 g) was mixed in 100 ml of toluene with 7 g of the above benzoyloxyacetaldehyde, a few crystals of ptoluenesulfonic acid added and the mixture place in an oil-bath at 120°C under N2. The formed ethanol was allowed to distill over, the mixture kept at 120°C for 30 min longer than cooled and washed with aqueous NaHCO3, dried and evaporated in vacuo. The residue was distilled in vacuo to yield 9.8 g of 2-benzoyloxymethyl-5-ethoxy-1,3-oxathiolane as a mixture of cis- and transisomers, boiling point 140-143°C/0.1 mm.
Cis- and trans-2-benzoyloxymethyl-5-cytosin-1'-yl-1,3-oxathiolane:
A mixture of 2.7 g of cytosine, 30 ml of hexamethyldisilazane (HMDS) and 0.3 ml of trimethylsilyl chloride (TMSCl) was heated under reflux under dry N2 untila clear solution resulted (3 L) and the excess reagents evaporated in vacuo. The remaining volatiles were removed under high vacuum, the solid residue taken up in 250 ml of dichlorethane and 5 g of the 2-benzoyloxymethyl-5-ethoxy-1,3-oxathiolane in 50 ml of dichloroethane added under dry argon followed by 4.7 ml of trimethylsilyl triflate. After 3 days of heating under reflux under argon, it was cooled and poured onto 300 ml of saturated aqueous NaHCO3. The organic layer was collected, the aqueous phase extracted with CH2Cl2and the combined extracts washed with water, dried and evaporated in vacuo. The residue was purified by chromatography on silica gel using CH2Cl2-CH3OH 9:1 as the eluant to give 2.5 g of a pure mixture of cis- and trans-2-benzoyloxymethyl-5-cytosin-1'-yl-1,3-oxathiolane in a 1:1 ratio. These were separated as the N-acetyl derivatives.
The preceding mixture of cis- and trans-2-benzoyloxymethyl-5-cytosin-1'-yl- 1,3-oxathiolane (2.5 g) in 100 ml of dry pyridine containing 0.1 g of 4- dimethylaminopyridine (DMAP) was treated with acetic anhydride (7 ml) at room temperature and after 16 h, the mixture was poured onto cold water followed by extraction with CH2Cl2. The extract was washed with water, dried, and evaporated in vacuo. Toluene was added to the residue, then evaporated in vacuo and the residual oil purified by chromatography on silica gel using EtOAc-CH3OH 99:1 as the eluant to yield 1.35 g of pure trans-2- benzoyloxymethyl-5-(N4-acetyl-cytosin-1'-yl)-1,3-oxathiolaneas the fast moving product and 1.20 g of pure cis-2-benzoyloxymethyl-5-cytosin-1'-yl- 1,3-oxathiolan as the slow moving component, melting point 158-160°C.
Cis- and trans-isomers of 2-hydroxymethyl-5-(cytosin-1'-yl)-1,3-oxathiolane was obtained by action of methanolic ammonia at 24°C.

brand name

Epivir (GlaxoSmithKline).

Therapeutic Function


Acquired resistance

A single codon change at position 184 in the HIV reverse transcriptase gene confers high-level resistance. The K65R mutation is also associated with resistance. In-vitro data indicate that lamivudine resistance may restore HIV sensitivity to zidovudine- and tenofovir-resistant virus.

General Description

Lamivudine is (-)-2',3'-dideoxy-3'-thiacytidine, (-)-β-L-(2R,5S)-1,3-oxathiolanylcytosine, 3TC, or (-)-(S)-ddC.Lamivudine is a synthetic nucleoside analog that differsfrom 2β,3β-dideoxycytidine (ddC) by the substitution of asulfur atom in place of a methylene group at the 3'-positionof the ribose ring. In early clinical trials, lamivudine exhibitedhighly promising antiretroviral activity against HIVand low toxicity in the dosages studied.Preliminarypharmacokinetic studies indicated that it exhibited goodoral bioavailability (F=~80%) and a plasma half-life of 2to 4 hours.

General Description

Lamivudine is a nucleoside analogue and reverse transcriptase inhibitor used in the therapy of human immunodeficiency virus (HIV) and hepatitis B virus (HBV) infection. Lamivudine is a very rare cause of clinically apparent drug induced liver injury, but is associated with flares of underlying hepatitis B during therapy or with abrupt withdrawal. Lamivudine (formerly known as 3TC) in combination with zidovudine is indicated for the treatment of HIV infection in patients who experience disease progression as evidenced by clinical and/or immunological test.

Pharmaceutical Applications

An analog of cytidine available for oral administration.

Biochem/physiol Actions

Lamivudine is a potent nucleoside analog reverse transcriptase inhibitor (nRTI). It is an analogue of cytidine, and can inhibit both types (1 and 2) of HIV reverse transcriptase as well as the reverse transcriptase of hepatitis B. It needs to be phosphorylated to its triphosphate form before it is active. 3TC-triphosphate also inhibits cellular DNA polymerase.


Oral absorption: 80–85%
Cmax, 300 mg once daily: 2.0 mg/L
Plasma half-life: 5–7 h
Volume of distribution: 1.3 L/kg
Plasma protein binding: <36%
It is rapidly absorbed and there is no significant difference in bioavailability when taken with food.
It penetrates moderately well into the CNS. The semen:plasma ratio is about 9.1 (2.3–16.1). It is secreted into breast milk.
Metabolism and excretion
Less than 10% of the administered dose undergoes hepatic metabolism. Over 70% of the dose is subject to renal clearance via active tubular secretion. Dosage adjustments are not routinely recommended in the presence of renal or hepatic impairment.


Lamivudine is rapidly absorbed after oral consumption. Fasted and non-fasted states do not interfere with lamivudine absorption; therefore, lamivudine can be administered with or without food. Binding of lamivudine to plasma proteins is <36%. The primary route of excretion is in the urine. The mean elimination half-life ranges from 5 to 7 hours. Decreased renal function increases the mean elimination half-life of lamivudine. Pharmokinetics effects of impaired renal function in pediatric patients are not known. Pharmokinetic properties of lamivudine have not been studied with respect to race, gender, or geriatrics.

Clinical Use

Lamivudine is indicated for the treatment of HIV when used in combination with other antiretroviral agents.A lower dose than that used to treat HIV is approved for the treatment of HBV. Although lamivudine initially improves histological and biochemical measures of hepatic function and reduces HBV DNA to below the limits of detection, withdrawal of the drug usually results in disease recurrence. Resistance appears in up to onethird of patients after 1 year of treatment.

Side effects

Lamivudine is relatively safe and non-toxic. Animal studies of very high doses did not result in any organ toxicity. In patients co-infected with HIV and HBV, cessation of lamivudine therapy may result in clinical and/or laboratory evidence of recurrent hepatic disease that may be more severe in patients with hepatic decompensation. Tests of liver function and inflammation and markers of HBV replication should be periodically monitored.
Lamivudine competes with emtricitabine for the enzymes involved in intracellular phosphorylation and co-administration is contraindicated.

Lamivudine Preparation Products And Raw materials

Raw materials

Preparation Products

Lamivudine Suppliers

Global( 502)Suppliers
Supplier Tel Fax Email Country ProdList Advantage
Coben pharmaceutical Co., Ltd United States 1 58
Sinoway Industrial co., ltd.
0592-5854960 CHINA 311 58
Frapp's ChemicalNFTZ Co., Ltd.
+86 (576) 8169-6106
+86 (576) 8169-6105 China 886 50
Beijing Cooperate Pharmaceutical Co.,Ltd
010-60279497 CHINA 1817 55
Henan Tianfu Chemical Co.,Ltd.
0371-55170693 China 22607 55
Hangzhou FandaChem Co.,Ltd.
+86-571-56059825 China 9156 55
Guangzhou PI PI Biotech Inc
020-81716319; China 3284 55
Hubei XinRunde Chemical Co., Ltd.
02783214688 CHINA 567 55
career henan chemical co
+86-0371-55982848 China 29953 58
Shaanxi Yikanglong Biotechnology Co., Ltd.
17791478691 CHINA 297 58

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View Lastest Price from Lamivudine manufacturers

Image Release date Product Price Min. Order Purity Supply Ability Manufacturer
2022-01-25 Lamivudine
2021-12-29 Lamivudine
2021-12-01 Lamivudine
US $10.00 / Kg/Drum 1KG 98% 10 ton Hebei Crovell Biotech Co Ltd

Lamivudine Spectrum

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