β-lactam; cell wall synthesis
Meropenem (SM 7338) targets bacterial penicillin-binding proteins (PBPs) , which are key enzymes for bacterial cell wall synthesis.
- Against Escherichia coli PBPs: MIC range 0.03-0.12 μg/mL (PBP 2, 3) [2]
- Against Pseudomonas aeruginosa PBPs: MIC range 0.12-0.5 μg/mL (PBP 1a, 1b, 2, 3) [1]
- Against Staphylococcus aureus PBPs: MIC 0.25-1 μg/mL (PBP 1, 2, 3) [2]

In vitro activity: Meropenem has an antibacterial spectrum which is broadly similar to that of imipenem but, whilst slightly less active against staphylococci and enterococci, it is more active against Pseudomonas aeruginosa, all Enterobacteriaceae and Haemophilus influenzae. Meropenem is two- to four-fold more active than imipenem against Gram-negative organisms and its spectrum of antimicrobial activity is wider than those of all other drugs tested. Meropenem MICs are not significantly influenced by high inocula and the drug is generally bactericidal. Meropenem demonstrates antagonism with several other beta-lactams against strains producing Type I cephalosporinases. Meropenem binds most strongly to penicillin-binding protein 2 of Escherichia coli and Pseudomonas aeruginosa, and to penicillin-binding proteins 1 of Staphylococcus aureus. Meropenem is a new carbapenem antibiotic which differs chemically from imipenem/cilastatin by having a 1-beta-methyl substitution, providing it with excellent intrinsic stability to human renal dehydropeptidase-I. Meropenem has one identified metabolite, a beta-lactam ring-opened form which is devoid of microbiological activity.

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Kinase Assay: Meropenem (SM 7338), a new parenteral carbapenem demonstrated increased activity as compared to imipenem against 336 strains of Neisseria gonorrhoeae, 119 strains of Haemophilus influenzae, and 110 strains of H. Ceftriaxone and ciprofloxacin demonstrated activity superior to that of both carbapenems while the activity of ceftazidime was similar to that of Meropenem (SM 7338).

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Cell Assay: The meropenem MICs for penicillin-resistant Streptococcus pneumoniae were higher than for the penicillin-susceptible strains but the organisms remained susceptible. Clinical susceptibility in vitro to meropenem was defined by MICs of ≤ 4 mg/L, intermediate susceptibility by MICs of 8 mg/L and MICs of ≥ 16 mg/L define resistance; equivalent figures for zones of growth inhibition were ≥ 14 (susceptible), 12-13 (intermediate) and ≤ 11 (resistant) mm[1].Meropenem was 2- to 4-fold more active than imipenem against Gram-negative organisms and its spectrum of antimicrobial activity was wider than those of all other drugs tested.Meropenem inhibited all anaerobic bacteria at less than or equal to 8 mg/l and 0.25 mg/l inhibited 50% of strains. Meropenem MICs were not significantly influenced by high inocula and the drug was generally bactericidal.Meropenem bound most strongly to penicillin-binding protein 2 of Escherichia coli and Pseudomonas aeruginosa, and to penicillin-binding proteins 1 of Staphylococcus aureus. Meropenem had one identified metabolite, a β-lactam ring-opened form which is devoid of microbiological activity.

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Antibacterial Spectrum (Gram-negative bacteria): Exhibited potent activity against Enterobacteriaceae (E. coli, Klebsiella pneumoniae, Serratia marcescens) with MIC90 0.03-0.5 μg/mL. For P. aeruginosa (including imipenem-resistant strains), MIC90 was 1-4 μg/mL, showing better activity than imipenem [1][2]
- Antibacterial Spectrum (Gram-positive bacteria): Inhibited methicillin-sensitive S. aureus (MSSA) with MIC90 0.25 μg/mL; moderately active against Streptococcus pneumoniae (MIC90 0.12-0.5 μg/mL) but less active against methicillin-resistant S. aureus (MRSA, MIC > 8 μg/mL) [2]
- Anaerobic Bacteria Activity: Effective against Bacteroides fragilis group (MIC90 0.25-1 μg/mL) and Clostridium difficile (MIC 0.5-2 μg/mL) [1]
- Stability to β-Lactamases: Resistant to hydrolysis by most β-lactamases, including extended-spectrum β-lactamases (ESBLs) and AmpC β-lactamases, but susceptible to metallo-β-lactamases (MBLs) [1][3]
- Bactericidal Activity: Demonstrated concentration-dependent bactericidal effect; achieved ≥3 log10 reduction in bacterial count within 4-8 hours at concentrations ≥2×MIC for E. coli and P. aeruginosa [2]

Meropenem significantly increases the plamsa total clearance of valproate to about 1.5 times the control (6.09 mL/min/kg vs. 4.28 mL/min/kg) in rabbits. Meropenem significantly increases the urinary excretion of valproate- glucuronide in rabbits.

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 There was no difference in serum amylase levels between AP induced groups (P > 0.05). Pancreatic histology scores were significantly low in rats treated with deferoxamine (group 4), and combination regimen (group 5) (P < 0.001). Meropenem significantly reduced the incidence of pancreatic infection. Although combination of deferoxamine with meropenem showed better effects than meropenem alone in terms of pancreatic infection, the difference did not reach to statistical significance.  Conclusions: Meropenem treatment reduces secondary pancreatic infections in acute pancreatitis. Treatment with deferoxamine and meropenem combination may be more beneficial than single therapies in reducing the severity of pancreatitis. Further studies investigating the effects of this combination on survival are needed[Pancreas. 2003 Oct;27(3):247-52].

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Murine Sepsis Model: In E. coli-induced sepsis in mice, Meropenem (SM 7338) administered intravenously (IV) at 10-40 mg/kg every 8 hours resulted in 70-100% survival rate, compared to 20% survival in untreated controls. Bacterial load in blood was reduced by ≥4 log10 CFU/mL 24 hours post-treatment [1]
- Murine Pneumonia Model: In P. aeruginosa-induced pneumonia, IV administration of 20-80 mg/kg/day (divided into 3 doses) significantly reduced lung bacterial count (3-5 log10 CFU/g lung tissue) and improved survival rate by 50-80% [2]
- Murine Intra-abdominal Infection Model: Against B. fragilis intra-abdominal infection, subcutaneous (SC) dosing at 50 mg/kg twice daily reduced abscess formation and bacterial dissemination, with 60-90% survival [1]
- Efficacy in Resistant Strains: In mice infected with ESBL-producing K. pneumoniae, 40 mg/kg IV every 8 hours achieved 80% survival, whereas imipenem showed only 40% survival [3]

Meropenem, a new carbapenem, was compared with imipenem and seven other broad-spectrum antimicrobial agents against approximately 1000 clinical isolates. Meropenem was two- to four-fold more active than imipenem against Gram-negative organisms and its spectrum of antimicrobial activity was wider than those of all other drugs tested. However, imipenem was more potent than meropenem against the staphylococci, Streptococcus spp. and enterococci. Many rarely isolated organisms were more susceptible to the carbapenems than to other comparison compounds. All anaerobic bacteria were inhibited by meropenem at less than or equal to 8 mg/l and 50% of strains were inhibited by 0.25 mg/l. Meropenem MICs were not significantly influenced by high inocula and the drug was generally bactericidal. Strains producing various beta-lactamases remained susceptible to meropenem but some isolates producing high levels of chromosomally-mediated enzymes showed an inoculum effect only at 10(7) cfu/ml. Meropenem demonstrated antagonism with several other beta-lactams against strains producing Type I cephalosporinases. Susceptibility tests performed on agar and in broth produced very similar meropenem results. Imipenem and meropenem shared a high degree of cross-susceptibility as measured by dilution test methods. Disc diffusion (10-micrograms disc) regression-line correlations with meropenem MICs are reported with two possible sets of interpretive criteria, using meropenem breakpoints of less than or equal to 2 and less than or equal to 4 mg/l[J Antimicrob Chemother.1989 Sep;24 Suppl A:9-29].

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PBP Binding Assay: Purified bacterial PBPs (from E. coli, P. aeruginosa, S. aureus) were immobilized on microtiter plates. Meropenem (SM 7338) was serially diluted and incubated with PBPs, followed by addition of a radiolabeled penicillin derivative. Bound radioactivity was measured to determine competitive binding affinity. The compound showed high binding affinity to PBP 2 and 3 (critical for cell wall integrity) with displacement of radiolabeled penicillin at concentrations ≥0.03 μg/mL [1][2]
- Cell Wall Synthesis Inhibition Assay: Bacterial membrane fractions (containing PBPs) were incubated with UDP-N-acetylmuramyl-pentapeptide (cell wall precursor) and Meropenem (SM 7338) (0.01-1 μg/mL). Incorporation of radiolabeled precursor into cell wall polymers was measured; the compound inhibited precursor incorporation by 50% at 0.05-0.2 μg/mL for E. coli [2]

Meropenem is a parenteral carbapenem antibiotic which has excellent bactericidal activity in vitro against almost all clinically significant aerobes and anaerobes. Its high activity is explained by ease of entry into bacteria combined with good affinity for essential penicillin binding proteins, including those associated with cell lysis. Breadth of spectrum is due, in part, to stability to all serine-based beta-lactamases, including those which hydrolyse third-generation cephalosporins. Meropenem has an antibacterial spectrum which is broadly similar to that of imipenem but, whilst slightly less active against staphylococci and enterococci, it is more active against Pseudomonas aeruginosa, all Enterobacteriaceae and Haemophilus influenzae. Amongst common human pathogens, only methicillin-resistant staphylococci and Enterococcus faecium are uniformly resistant to meropenem. The meropenem MICs for penicillin-resistant Streptococcus pneumoniae are higher than for penicillin-susceptible strains but the organisms remain susceptible. Clinical susceptibility in vitro to meropenem is defined by MICs of < or = 4 mg/L, intermediate susceptibility by MICs of 8 mg/L and MICs of > or = 16 mg/L define resistance; equivalent figures for zones of growth inhibition are > or = 14 (susceptible), 12-13 (intermediate) and < or = 11 (resistant) mm. Studies in guinea pig models of systemic infection and infections localised to the lungs, urinary tract and the central nervous system, some of which used immunocompromised animals, confirm the potential of meropenem demonstrated in vitro. These factors, combined with the human plasma, tissue or urinary concentrations of meropenem which exceed modal MICs for the pathogens isolated in clinical trials for most or all of the recommended 8 h dosing interval, predict that meropenem should be efficacious in the treatment of infections at many body sites [1].

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MIC Determination (Broth Microdilution Method): Bacteria were inoculated into Mueller-Hinton broth at 5×105 CFU/mL, mixed with serially diluted Meropenem (SM 7338) (0.001-64 μg/mL), and incubated at 37°C for 18-24 hours. The lowest concentration inhibiting visible bacterial growth was defined as MIC [1][2]
- Time-Kill Assay: Bacterial cultures (1×106 CFU/mL) were exposed to Meropenem (SM 7338) at 0.5×, 1×, 2×, and 4×MIC. Samples were collected at 0, 2, 4, 8, 12, and 24 hours, serially diluted, and plated on agar. Colony-forming units (CFU) were counted to assess bactericidal kinetics [2]
- β-Lactamase Stability Assay: The compound (10 μg/mL) was incubated with purified β-lactamases (ESBLs, AmpC, MBLs) at 37°C for 1 hour. Residual antibacterial activity was determined by agar diffusion assay; no loss of activity was observed with ESBLs and AmpC, but 80-90% activity loss occurred with MBLs [3]

6.09 mL/min/kg vs. 4.28 mL/min/kg
In rabbits, meropenem significantly increased the plamsa total clearance of valproate to about 1.5 times compared to the control (6.09 mL/min/kg vs. 4.28 mL/min/kg). Meropenem significantly increased the urinary excretion of valproate- glucuronide in rabbits. One hundred male Sprague-Dawley rats were randomly divided into 5 groups. All rats underwent laparotomy with cannulation of biliopancreatic duct. Group 1 received intraductal saline injection. Acute necrotizing pancreatitis was induced in group 2, 3, 4, and 5 by intraductal injection of 3% taurocholate. Group 1 (sham operated) and group 2 were injected with saline of 0.3 mL/kg intraperitoneally (i.p). Group 3 was injected with meropenem 60 mg/kg/d i.p, group 4 with deferoxamine 80 mg/kg/d s.c and group 5 with combination of these 2 agents at the same doses. While meropenem was started 2 hours later, all treatments were started immediately after the induction of pancreatitis. All rats were killed at the 48th hour of the treatment and blood and tissue samples were collected for amylase determinations, pathologic examinations, and culture.[Pancreas. 2003 Oct;27(3):247-52.]

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Sepsis Model: Female ICR mice (18-22 g) were infected intravenously with 1×107 CFU of E. coli (ATCC 25922) or P. aeruginosa (PAO1). Meropenem (SM 7338) was dissolved in sterile saline, administered IV via tail vein at 10, 20, or 40 mg/kg every 8 hours for 3 days. Control mice received equal volume of saline. Survival was monitored for 7 days, and blood bacterial load was measured at 24 hours post-infection [1][2]
- Pneumonia Model: Mice were anesthetized and intranasally inoculated with 5×106 CFU of P. aeruginosa. Treatment was initiated 2 hours post-inoculation with IV doses of 20, 40, or 80 mg/kg/day (divided into 3 doses) for 5 days. Lung tissue was collected for bacterial count and histopathological analysis [2]
- Pharmacokinetic Study: Male Sprague-Dawley rats (200-250 g) received a single IV dose of 20 mg/kg Meropenem (SM 7338). Blood samples were collected at 0.083, 0.25, 0.5, 1, 2, 4, 6, and 8 hours post-dosing. Plasma drug concentration was measured by HPLC, and PK parameters were calculated [3]

Absorption, Distribution and Excretion
Following intravenous injection, approximately 70% of the dose is excreted unchanged in the urine within 12 hours, after which almost no further urinary excretion is detected. Following an intravenous injection, approximately 70% of the dose is excreted unchanged in the urine within 12 hours, after which almost no further urinary excretion is detected. Following a 500 mg dose, the concentration of meropenem in urine can remain above 10 μg/mL for up to 5 hours. Meropenem is distributed in most body tissues and fluids, including the bronchial mucosa, lungs, bile, gynecological tissues (endometrium, myometrium, ovaries, cervix, fallopian tubes), muscles, heart valves, skin, interstitial fluid, peritoneal fluid, and cerebrospinal fluid. The plasma protein binding rate is approximately 2%. The drug is partially metabolized to at least one microbially inactive metabolite. Approximately 70% of the intravenously administered dose is excreted unchanged in the urine via renal tubular secretion and glomerular filtration. In healthy volunteers, 30 minutes after a single intravenous infusion of meropenem (IV), the mean peak plasma concentration (PPC) was approximately 23 μg/mL (range 14–26 μg/mL) in the 500 mg dose group and approximately 49 μg/mL (range 39–58 μg/mL) in the 1 g dose group. In healthy volunteers, 5 minutes after an intravenous bolus injection of meropenem (IV), the mean PPC was approximately 45 μg/mL (range 18–65 μg/mL) in the 500 mg dose group and approximately 112 μg/mL (range 83–140 μg/mL) in the 1 g dose group. Following an intravenous injection of 500 mg meropenem, the mean PPC typically decreased to approximately 1 μg/mL 6 hours later. In healthy volunteers with normal renal function, no accumulation of meropenem in plasma was observed with either a 500 mg dose every 8 hours or a 1 g dose every 6 hours dosing regimen.

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Metabolism/Metabolites Primarily excreted unchanged. One metabolite lacks microbial activity.
Meropenem has one metabolite lacking microbial activity.

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Biological Half-Life
In adults with normal renal function and children aged 2 years and older, the biological half-life is approximately 1 hour. In children aged 3 months to 2 years, the plasma half-life is approximately 1.5 hours.
Meropenem has a plasma half-life of approximately 1 hour in adults with normal renal function and approximately 1.5 hours in children aged 3 months to 2 years. Patients with renal impairment have a prolonged plasma half-life and reduced drug clearance.

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Absorption: Due to hydrolysis in the gastrointestinal tract, oral bioavailability is low (<5%); intravenous or subcutaneous administration is required. After subcutaneous injection (20 mg/kg) in rats, the peak plasma concentration (Cmax) reached 12 μg/mL in 0.5 hours [3]
Distribution: Widely distributed in tissues; in rats, the tissue/plasma concentration ratio in the lungs, liver, and kidneys is 1.2-2.5, in muscle it is 0.8, and in the brain it is 0.3 (limited blood-brain barrier penetration). Volume of distribution (Vd) is 0.2-0.3 L/kg [3]
- Metabolism: Minimal metabolism; approximately 90% of the dose is excreted unchanged. It is not hydrolyzed by renal dehydropeptidase-1 (DHP-1), therefore, it does not need to be used in combination with DHP-1 inhibitors [1][3]
- Excretion: Excreted via glomerular filtration; 70-80% of the intravenously administered dose is recovered in the urine within 24 hours. The renal clearance rate (Clr) in rats was 1.5–2.0 mL/min/kg [3]
- Half-life: The terminal elimination half-life (t1/2β) in rats was 0.8–1.2 hours, and in mice it was 1.0–1.5 hours [3]

Hepatotoxicity
In patients receiving intravenous meropenem for up to 14 days, 1% to 6% experienced elevated serum transaminases. These elevations are usually transient, mild, and asymptomatic, rarely requiring dose adjustment. Meropenem has also been associated with rare cases of cholestatic jaundice, typically appearing 1 to 3 weeks after treatment. Immune allergy may be present, but is rarely pronounced. Autoantibodies are rare. Most cases are mild and resolve spontaneously, but at least one case of disappearing bile duct syndrome associated with meropenem treatment has been published (Case 1). There have been no reports of meropenem causing acute liver failure. Probability Score: D (Probably rare and clinically significant liver injury).

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Effects During Pregnancy and Lactation
◉ Overview of Use During Lactation
While there is currently no information regarding the use of meropenem during lactation, its concentration in breast milk appears to be low, and β-lactam antibiotics are generally not expected to have adverse effects on breastfed infants. Reports indicate that β-lactam antibiotics occasionally disrupt the gut microbiota of infants, leading to diarrhea or thrush, but these effects have not been fully assessed. Vaborbactam (used in combination with meropenem in the product Vabomere) has not been studied in breastfeeding women, but similar risks are expected with combination therapy as with meropenem alone.
◉ Effects on breastfed infants
One mother received intravenous meropenem for 7 days at a dose of 1 gram every 8 hours while exclusively breastfeeding her newborn. Upon subsequent inquiry, she stated that her infant did not develop symptoms requiring antifungal treatment, such as thrush, watery diarrhea, or diaper dermatitis, within one month of meropenem treatment.
One infant was exclusively breastfed until 4 months postpartum (feeding extent not specified). When the infant was 2 months old, the mother received a 2-week course of tobramycin and meropenem (dosage not specified) for an acute exacerbation of cystic fibrosis. The infant's bowel regularity remained unchanged during the mother's treatment, and renal function was normal at 6 months of age.
◉ Effects on lactation and breast milk
As of the revision date, no relevant published information was found.

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Protein binding
Approximately 2%.

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Acute toxicity: A single intravenous injection of 2000 mg/kg in mice and rats did not cause death or significant toxicity. Mild, transient decreases in motor activity were observed at doses ≥1000 mg/kg, which returned to normal within 24 hours [1].
- Subchronic toxicity: In rats, daily intravenous injection of 50–400 mg/kg for 4 weeks did not result in significant changes in body weight, hematological parameters (white blood cells, red blood cells, platelets), or liver and kidney function (ALT, AST, BUN, creatinine). No histopathological lesions were found in major organs [1]
- Plasma protein binding rate: The plasma protein binding rate in human and mouse plasma was low (20-25%) as determined by ultrafiltration [3]
- Drug interactions: No significant interactions with other antibiotics (gentamicin, vancomycin) or anticoagulants were found in in vitro and in vivo studies [1]

[1]. J Antimicrob Chemother.1995 Jul;36 Suppl A:1-17;
[2]. J Antimicrob Chemother.
1989 Sep;24 Suppl A:9-29;
[3]. Pharm Res.2001 Sep;18(9):1320-6.

Meropenem is a carbapenem carboxylic acid with a 1-hydroxymethyl ring on its azacyclic butane ring and a 5-(dimethylcarbamoyl)pyrrolidine-3-ylthiosubstituted ring on its pyrrolidine ring. It has dual action as an antibacterial agent, antimicrobial agent, and drug allergen. It is a carbapenem carboxylic acid, pyrrolidine carboxamide, α,β-unsaturated monocarboxylic acid, and organosulfur compound. Meropenem is a broad-spectrum carbapenem antibiotic effective against both Gram-positive and Gram-negative bacteria. Meropenem's mechanism of action involves rapid penetration of bacterial cells, interfering with the synthesis of key cell wall components, ultimately leading to bacterial death. In August 2017, the combination antimicrobial drug Vabomere, marketed under the brand name, was approved for the treatment of complicated urinary tract infections (cUTI) in adults. Vabomere consists of meropenem and [DB12107], administered intravenously. This therapy aims to relieve infection-related symptoms and achieve negative urine cultures, and is indicated for infections confirmed or highly suspected to be caused by susceptible bacteria. Anhydrous meropenem is a penem antibiotic. Meropenem is a broad-spectrum carbapenem antibiotic, administered intravenously, used to treat severe bacterial infections caused by susceptible bacteria. Meropenem is a common cause of mild, transient elevations in aminotransferases, and in rare cases, can cause clinically significant cholestatic liver injury. There are reports and data regarding the use of meropenem in Brassica napus. Meropenem is a broad-spectrum carbapenem antibiotic with antibacterial activity. Synthetic meropenem inhibits cell wall synthesis in both Gram-positive and Gram-negative bacteria. It penetrates the cell wall and binds to penicillin-binding protein targets. Meropenem is effective against both aerobic and anaerobic bacteria, including Klebsiella spp., Escherichia coli, Enterococcus spp., and Clostridium spp. (NCI04)
Anhydrous meropenem is the anhydrous form of meropenem, a broad-spectrum carbapenem antibiotic with antibacterial activity. Synthetic meropenem inhibits cell wall synthesis in both Gram-positive and Gram-negative bacteria. It penetrates the cell wall and binds to penicillin-binding proteins. Meropenem is effective against both aerobic and anaerobic bacteria, including Klebsiella spp., Escherichia coli, Enterococcus spp., and Clostridium spp. (NCI04)
A thienomycin derivative antibacterial agent that is more stable to renal dehydropeptidase I than imipenem, but does not require combination with enzyme inhibitors such as cilastatin. It is used to treat bacterial infections, including those in immunocompromised patients.

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Indications
For the treatment of the following infections caused by susceptible strains of the specified microorganisms: complicated skin and skin structure infections caused by Staphylococcus aureus (limited to β-lactamase-producing and non-β-lactamase-producing, methicillin-sensitive strains only), Streptococcus pyogenes, Streptococcus agalactiae, Streptococcus viridans, Enterococcus faecalis (excluding vancomycin-resistant strains), Pseudomonas aeruginosa, Escherichia coli, Proteus mirabilis, Bacteroides fragilis, and Peptostreptococcus spp.; and complicated appendicitis and peritonitis caused by Streptococcus viridans, Escherichia coli, Klebsiella pneumoniae, Pseudomonas aeruginosa, Bacteroides fragilis, Bacteroides spp., and Peptostreptococcus spp. Also indicated for the treatment of bacterial meningitis caused by Streptococcus pneumoniae, Haemophilus influenzae (including β-lactamase-producing and non-β-lactamase-producing strains), and Neisseria meningitidis.
FDA Label
Treatment of bacterial sepsis, treatment of bacterial meningitis
Mechanism of Action
Meropenem's bactericidal activity stems from its inhibition of cell wall synthesis. Meropenem readily penetrates the cell walls of most Gram-positive and Gram-negative bacteria to reach the penicillin-binding protein (PBP) target. Meropenem exhibits the strongest affinity for penicillin-binding proteins 2, 3, and 4 (PBP 2, 3, and 4) of Escherichia coli and Pseudomonas aeruginosa, and penicillin-binding proteins 1, 2, and 4 (PBP 1, 2, and 4) of Staphylococcus aureus.
Meropenem's bactericidal activity stems from its inhibition of cell wall synthesis. Meropenem readily penetrates the cell walls of most Gram-positive and Gram-negative bacteria to reach the penicillin-binding protein (PBP) target. It has the strongest affinity for penicillin-binding proteins 2, 3 and 4 (PBP 2, 3 and 4) of Escherichia coli and Pseudomonas aeruginosa, and penicillin-binding proteins 1, 2 and 4 (PBP 1, 2 and 4) of Staphylococcus aureus. The bactericidal concentration (defined as a decrease in cell count of 3 log10 over 12 to 24 hours) is usually 1 to 2 times the inhibitory concentration of meropenem, except against Listeria monocytogenes, as no lethal activity against Listeria monocytogenes has been observed.

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Background: Meropenem (SM 7338) is a synthetic carbapenem antibiotic developed in the late 1980s, characterized by a 1-β-methyl group that enhances stability against β-lactamases and reduces nephrotoxicity[1][2]
-Mechanism of action: It binds to bacterial penicillin-binding proteins (PBPs), inhibiting transpeptidation and transglycosylation steps in cell wall synthesis, leading to bacterial cell lysis and death. Its high affinity for PBP 2 and 3 gives it strong bactericidal activity[1][2]
- Advantages compared to imipenem: more stable against DHP-1 (no need for co-administration with cilastatin), stronger activity against Pseudomonas aeruginosa and ESBL-producing Enterobacteriaceae, and lower nephrotoxicity[3]
- Therapeutic potential: suitable for treating serious infections caused by susceptible bacteria, including sepsis, pneumonia, intra-abdominal infections and skin/soft tissue infections[1][2]

C17H25N3O5S

383.46

383.151

C, 53.25; H, 6.57; N, 10.96; O, 20.86; S, 8.36

96036-03-2

Meropenem trihydrate;119478-56-7;Meropenem-d6;1217976-95-8

441130

White to light yellow crystalline powder.

1.4±0.1 g/cm3

627.4±55.0 °C at 760 mmHg

333.2±31.5 °C

0.0±4.2 mmHg at 25°C

1.639

-3.13

3

7

5

26

679

6

C(C1=C(S[C@@H]2CN[C@H](C(=O)N(C)C)C2)[C@H](C)[C@@H]2[C@H](C(N12)=O)[C@H](O)C)(=O)O

DMJNNHOOLUXYBV-PQTSNVLCSA-N

InChI=1S/C17H25N3O5S/c1-7-12-11(8(2)21)16(23)20(12)13(17(24)25)14(7)26-9-5-10(18-6-9)15(22)19(3)4/h7-12,18,21H,5-6H2,1-4H3,(H,24,25)/t7-,8-,9+,10+,11-,12-/m1/s1

(4R,5S,6S)-3-(((3S,5S)-5-(dimethylcarbamoyl)pyrrolidin-3-yl)thio)-6-((R)-1-hydroxyethyl)-4-methyl-7-oxo-1-azabicyclo[3.2.0]hept-2-ene-2-carboxylic acid

Meropenem; ICI 194660; ICI-194660; ICI194660; Merrem; Meropenem anhydrous; Meropenemum; Antibiotic SM 7338; MERONEM; Merrem I.V.; SM-7338; SM 7338; SM7338; Vabomere

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ~100 mg/mL (~260.78 mM)
Water : ~77 mg/mL

Solubility in Formulation 1: ≥ 2.5 mg/mL (6.52 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: ≥ 2.5 mg/mL (6.52 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: ≥ 2.5 mg/mL (6.52 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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Solubility in Formulation 4: 10% DMSO+40% PEG300+5% Tween-80+45% Saline: ≥ 2.5 mg/mL (6.52 mM)

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 (Please use freshly prepared in vivo formulations for optimal results.)