Tetracycline
Omadacycline is a novel, aminomethyl tetracycline antibiotic being developed for oral and intravenous (IV) administration to treat community-acquired bacterial infections such as acute bacterial skin and skin structure infections (ABSSSI), community-acquired bacterial pneumonia (CABP), and urinary tract infections (UTI). In vitro, omadacycline has activity against Gram-positive and Gram-negative aerobes, anaerobes, and atypical pathogens including Legionella and Chlamydia spp. Omadacycline offers once daily oral and IV dosing and a clinical tolerability and safety profile that compares favorably with contemporary antibiotics used across serious community-acquired infections where resistance has rendered many less effective. In studies in patients with complicated skin and skin structure infections, including those with MRSA infections, omadacycline exhibited an efficacy and tolerability profile that was comparable to linezolid. Ongoing and planned clinical studies are evaluating omadacycline as monotherapy for treating serious community-acquired bacterial infections including Acute Bacterial Skin and Skin Structure Infections (ABSSSI) and Community-Acquired Bacterial Pneumonia (CABP). This review provides an overview of the discovery, microbiology, nonclinical data, and available clinical safety and efficacy data for omadacycline, with reference to other contemporary tetracycline-derived antibiotics.

Omadacycline is a novel, aminomethyl tetracycline antibiotic being developed for oral and intravenous (IV) administration to treat community-acquired bacterial infections such as acute bacterial skin and skin structure infections (ABSSSI), community-acquired bacterial pneumonia (CABP), and urinary tract infections (UTI). In vitro, omadacycline has activity against Gram-positive and Gram-negative aerobes, anaerobes, and atypical pathogens including Legionella and Chlamydia spp. Omadacycline offers once daily oral and IV dosing and a clinical tolerability and safety profile that compares favorably with contemporary antibiotics used across serious community-acquired infections where resistance has rendered many less effective. In studies in patients with complicated skin and skin structure infections, including those with MRSA infections, omadacycline exhibited an efficacy and tolerability profile that was comparable to linezolid. Ongoing and planned clinical studies are evaluating omadacycline as monotherapy for treating serious community-acquired bacterial infections including Acute Bacterial Skin and Skin Structure Infections (ABSSSI) and Community-Acquired Bacterial Pneumonia (CABP). This review provides an overview of the discovery, microbiology, nonclinical data, and available clinical safety and efficacy data for omadacycline, with reference to other contemporary tetracycline-derived antibiotics.

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Omadacycline demonstrated broad-spectrum in vitro antibacterial activity against a wide panel of Gram-positive and select Gram-negative clinical isolates. [1]
Against Staphylococcus aureus (55 isolates), the MIC range was ≤0.06–1 µg/ml, with MIC50 and MIC90 values of 0.125 µg/ml and 0.5 µg/ml, respectively. It was active against methicillin-resistant S. aureus (MRSA, 39 isolates) with an MIC90 of 0.5 µg/ml. [1]
Against Enterococcus faecalis (31 isolates) and Enterococcus faecium (24 isolates), the MIC90 for Omadacycline was 0.5 µg/ml for both. It maintained activity against vancomycin-resistant E. faecium (VRE, 19 isolates) with an MIC90 of 0.5 µg/ml. [1]
Against Streptococcus pneumoniae (41 isolates), including penicillin-resistant and multidrug-resistant strains, Omadacycline showed potent activity with an MIC90 of 0.125 µg/ml. [1]
Omadacycline was active against beta-hemolytic streptococci (S. pyogenes and S. agalactiae) with MIC90 values of 0.25 µg/ml and 0.125 µg/ml, respectively. [1]
Against Gram-negative bacteria, Omadacycline exhibited activity against Escherichia coli (MIC90 = 2 µg/ml), Klebsiella pneumoniae (MIC90 = 4 µg/ml), and Haemophilus influenzae (MIC90 = 2 µg/ml). [1]
Omadacycline retained activity against bacterial strains harboring major tetracycline resistance mechanisms, including ribosomal protection genes [e.g., tet(M), tet(O), tet(S)] and efflux pump genes [e.g., tet(K), tet(L), tet(A)]. For example, against 19 S. aureus isolates carrying tet(M), the MIC range was 0.125–1 µg/ml. [1]
Multiplex PCR was used to confirm the presence of specific tetracycline resistance genes in the tested strains. [1]

In vivo efficacy of omadacycline is demonstrated using an intraperitoneal infection model in mice. A single intravenous dose of omadacycline exhibits efficacy against Streptococcus pneumoniae, Escherichia coli, and Staphylococcus aureus, including tet (M) and tet (K) efflux-containing strains and MRSA strains. The 50% effective doses (ED50s) for Streptococcus pneumoniae obtained ranged from 0.45 mg/kg to 3.39 mg/kg, the ED50s for Staphylococcus aureus obtained ranges from 0.30 mg/kg to 1.74 mg/kg, and the ED50 for Escherichia coli is 2.02 mg/kg.

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In vivo efficacy of omadacycline was demonstrated using an intraperitoneal infection model in mice. A single intravenous dose of omadacycline exhibited efficacy against Streptococcus pneumoniae, Escherichia coli, and Staphylococcus aureus, including tet(M) and tet(K) efflux-containing strains and MRSA strains. The 50% effective doses (ED50s) for Streptococcus pneumoniae obtained ranged from 0.45 mg/kg to 3.39 mg/kg, the ED50s for Staphylococcus aureus obtained ranged from 0.30 mg/kg to 1.74 mg/kg, and the ED50 for Escherichia coli was 2.02 mg/kg. These results demonstrate potent in vivo efficacy including activity against strains containing common resistance determinants. Omadacycline demonstrated in vitro activity against a broad range of Gram-positive and select Gram-negative pathogens, including resistance determinant-containing strains, and this activity translated to potent efficacy in vivo[1].

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The efficacy of a single intravenous dose of Omadacycline was evaluated in a murine lethal intraperitoneal infection model against various bacterial strains. [1]
Against Streptococcus pneumoniae strains, the 50% effective dose (ED50) values for Omadacycline ranged from 0.45 mg/kg to 3.34 mg/kg. It was effective against both tetracycline-sensitive (e.g., PBS1339, ED50 = 3.34 mg/kg) and tetracycline-resistant strains (e.g., 700905 carrying tet(M), ED50 = 0.45 mg/kg). [1]
Against Staphylococcus aureus strains, the ED50 values for Omadacycline ranged from 0.30 mg/kg to 1.74 mg/kg. It showed efficacy against methicillin-sensitive (e.g., 29213, ED50 = 1.74 mg/kg), methicillin-resistant (e.g., USA300, ED50 = 0.90 mg/kg), and tetracycline-resistant strains (e.g., MRSA5 carrying tet(M), ED50 = 0.30 mg/kg). [1]
Omadacycline also demonstrated in vivo efficacy against a tetracycline-sensitive Escherichia coli strain (PBS1478) with an ED50 of 2.02 mg/kg. [1]
In these studies, Omadacycline was often comparable or superior in efficacy (lower ED50) to comparator antibiotics such as vancomycin, linezolid, doxycycline, and tigecycline, particularly against strains carrying resistance determinants. [1]

In vitro stability and drug–drug interaction potential of omadacycline[2]
The stability of omadacycline (4.8 and 48 μM) was assessed in human microsomes and hepatocytes. After 30 min incubation of omadacycline in human microsomes, >90% of omadacycline was recovered intact. Similarly, after incubation of omadacycline up to 24 h in human hepatocytes, >86% was recovered intact. These results indicate that omadacycline is not metabolized to any significant extent.The potential for drug-drug-interactions with omadacycline was assessed using either pooled human liver microsome preparations, S9, liver cytosol, or recombinant flavin monooxygenases (FMO1, FMO3, FMO5). Induction of CYP450 isozymes was evaluated in primary human hepatocytes incubated with omadacycline 1–100 μM and a substrate probe for 24 and 48 h. Inhibition of CYP450 isozymes was evaluated with pooled human microsomes at omadacycline concentrations of 1–50 μM and isozyme specific substrates at concentrations approximating the Km of each substrate. Isozymes evaluated included CYP 1A1, 1A2, 1B1, 2A6, 2B6, 2C8, 2C9, 2C19, 2D6, 2E1, 2J2, and 3A4/5.Omadacycline did not induce CYP isozymes, and no or minimal (<40% of maximal positive control response) induction of their mRNAs was observed. Omadacycline demonstrated no significant inhibition of CYP isozyme activity. In addition, there was no time-dependent inhibition of omadacycline or its possible metabolites for CYP1A2 2C9, 2D6 or 3A4/5.

The omadacycline MIC90s for MRSA, VRE, and beta-hemolytic streptococci are 1.0 μg/mL, 0.25 μg/mL, and 0.5 μg/mL, respectively, and the omadacycline MIC90s for PRSP and H. influenzae are 0.25 μg/ml and 2.0 μg/mL, respectively. Omadacycline is active against organisms demonstrating the two major mechanisms of resistance, ribosomal protection and active tetracycline efflux. Omadacycline inhibits protein synthesis while having no significant effect on RNA, DNA and peptidoglycan synthesis. Further, omadacycline binds to the tetracycline binding site on the 30S subunit of the bacterial ribosome with enhanced binding similar to tigecycline based on additional molecular interactions.

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The primary cell-based assays described are standard broth microdilution antimicrobial susceptibility tests performed according to established guidelines to determine Minimum Inhibitory Concentrations (MICs). [1]
Briefly, bacterial isolates were subcultured onto appropriate solid media prior to testing. MICs were determined using broth microdilution methods. The tests were performed in suitable broth media, with horse or sheep blood supplementation added for fastidious organisms. Serial dilutions of antibiotics were prepared in microtiter plates, inoculated with a standardized bacterial suspension, and incubated. The MIC was defined as the lowest concentration that prevented visible growth. [1]
A multiplex PCR assay was used to detect and identify specific tetracycline resistance genes (tet(K), tet(L), tet(A), tet(B), tet(M), tet(O), tet(S)) in the bacterial strains used for in vitro testing. This was not a cell viability assay but a molecular characterization step. [1]

0.45 mg/kg to 3.39 mg/kg; i.p. Mice Systemic i.p. challenge model. Six-week-old, specific-pathogen-free, male CD-1 mice, weighing 18 to 30 g were used for all experiments. At 1 h postinfection (p.i.), mice were dosed intravenously (i.v.) with omadacycline or comparator compounds of interest, dissolved in sterile saline for injection at a volume of 10 ml/kg. All drug doses were formulated fresh immediately prior to administration and adjusted to account for percent activity. A minimum of four dose levels were tested per experiment with 5 mice/group. The typical doses tested ranged from 0.11 to 18 mg/kg of body weight, with exceptions for comparators that required significantly higher or lower doses to achieve 50% efficacy (dose range minimum-maximum, 0.08 to 54 mg/kg). Each study also included an untreated control group. Mice were housed in filter-topped cages in an isolated room and monitored for morbidity at least every 24 h for 7 days. Efficacy was determined by calculating the 50% effective dose (ED50) for all drugs tested. The ED50 is defined as the dose required to achieve 50% survival at 7 days p.i. and was estimated when possible using the formula y = 1/[1 + 10(log(k)-log(x)× 4.2)], where k = 0.5, by nonlinear regression analysis with Prism, version 3.0 software. [1]

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A systemic intraperitoneal (i.p.) challenge model in mice was used to evaluate the in vivo efficacy of Omadacycline. [1]
Six-week-old, specific-pathogen-free, male CD-1 mice were used. Animals were acclimated for one week before experiments. [1]
Bacterial cultures (S. pneumoniae, S. aureus, E. coli) were grown to appropriate densities. Bacterial suspensions were serially diluted in sterile phosphate-buffered saline (PBS) to achieve the desired infectious dose for each experiment. The actual dose was confirmed by plating and colony counting. [1]
Septicemia was induced by intraperitoneally injecting mice with 500 µL of a bacterial suspension containing a defined number of colony-forming units (CFU), mixed in a 4.5% bacteriological mucin solution to enhance infection. [1]
At 1 hour post-infection, mice were treated intravenously (i.v.) with a single dose of Omadacycline or comparator antibiotics. Drugs were dissolved in sterile saline for injection. The dosing volume was 10 ml/kg. Drug solutions were formulated fresh immediately prior to administration. [1]
A minimum of four dose levels were tested per experiment with 5 mice per group. Typical dose ranges tested were from 0.11 to 18 mg/kg, with exceptions for some comparators. Each study included an untreated control group. [1]
Mice were monitored for morbidity at least every 24 hours for 7 days post-infection. The primary efficacy endpoint was survival at 7 days. The 50% effective dose (ED50), defined as the dose required to achieve 50% survival at 7 days, was calculated using nonlinear regression analysis. [1]

Omalia cycline's pharmacokinetic profile best conforms to a linear three-compartment model, with zero-order kinetics for intravenous infusion and first-order kinetics for oral administration, taking into account the transport compartment to explain delayed absorption. The volume of distribution (Vd) of omaalia cycline is 190–204 L, the terminal elimination half-life (t½) is 13.5–17.1 h, the total clearance (CLT) is 8.8–10.6 L/h, and the protein binding rate in healthy subjects is 21.3%. The estimated oral bioavailability of omaalia cycline is 34.5%. Following a single oral dose of 300 mg (bioequivalent to 100 mg intravenously) of omaalia cycline, the peak plasma concentration (Cmax) in fasting subjects is 0.5–0.6 mg/L, and the area under the plasma concentration-time curve (AUC0–∞) is 9.6–11.9 mg·h/L. The area under the free plasma concentration-time curve divided by the minimum inhibitory concentration (fAUC24h/MIC) has been identified as a pharmacodynamic parameter for predicting the antibacterial efficacy of omalicycline. Multiple animal models, including neutropenic mouse models of lung infection, thigh infection, and intraperitoneal infection, have demonstrated the in vivo antibacterial efficacy of omalicycline. A phase II clinical trial for complicated skin and soft tissue infections (cSSSI) and three phase III clinical trials for acute bacterial skin and soft tissue infections (ABSSSI) and community-acquired bacterial pneumonia (CABP) have confirmed the safety and efficacy of omalicycline. The phase III clinical trials OASIS-1 (ABSSSI), OASIS-2 (ABSSSI), and OPTIC (CABP) demonstrated that omalicycline is non-inferior to linezolid (OASIS-1, OASIS-2) and moxifloxacin (OPTIC) in the treatment of ABSSSI and CABP, respectively. Currently, omalicycline is approved by the FDA for the treatment of ABSSSI and CABP. Phase II clinical trials for patients with acute cystitis and acute pyelonephritis are underway. Mild, transient gastrointestinal reactions are the main adverse reactions of omalicycline. Based on clinical trial data to date, the adverse reaction profile of omalicycline is similar to that of the study control drugs linezolid and moxifloxacin. Unlike tigecycline and eracycline, omalicycline is available in oral formulations, allowing for a gradual transition from intravenous to oral formulations, which may help patients be discharged earlier, receive outpatient treatment, and save on medical costs. Omalicycline has potential role in antimicrobial management regimens for the treatment of infections caused by drug-resistant and multidrug-resistant Gram-positive bacteria, including methicillin-resistant Staphylococcus aureus (MRSA), and Gram-negative pathogens. [https://pubmed.ncbi.nlm.nih.gov/31970713/]

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Omalicycline is metabolically stable. [1]
Omalicycline exhibits low plasma protein binding at all tested concentrations and species. [1]
In a Phase I ADME study in humans, no metabolites of omalicycline were isolated, indicating that its metabolism is stable. [1]
Omalicycline was observed to be excreted in a balanced manner through the intestines and urinary system. High concentrations of the drug were detected in urine. [1]
Omalicycline can be bioavailable in humans via oral and intravenous routes. [1]
The bioavailability of omalicycline via oral administration in rodents is significantly lower than that in humans and other non-rodents. Therefore, an efficacy study was conducted in mice via intravenous administration. [1]

Effects During Pregnancy and Lactation
◉ Overview of Use During Lactation
There is currently no information regarding the use of omalicycline during lactation. It is unclear how much omalicycline is excreted into breast milk, but even under optimal conditions, the oral absorption rate is only about 35%, and the amount of omalicycline in breast milk may be even lower due to its calcium content. The manufacturer states that breastfeeding is not recommended during treatment and for 4 days after the last dose. If the infant is being breastfed, the infant's gut microbiota should be monitored for any impact, such as diarrhea, candidiasis (e.g., thrush, diaper rash), or rare hematochezia (suggesting possible antibiotic-associated colitis). Prolonged or repeated use during lactation should theoretically be avoided.
◉ Effects on Breastfed Infants
No published information found as of the revision date.
◉ Effects on Lactation and Breast Milk
No published information found as of the revision date.

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In a phase II study of patients with complicated skin and soft tissue infections, both oral and intravenous omalicycline showed good tolerability. [1]

[1]. Antimicrob Agents Chemother.2014;58(2):1127-35.

[2]. Bioorg Med Chem.2016 Dec 15;24(24):6409-6419.

[3]. Pharmaceuticals (Basel). 2019 Apr 21;12(2):63.

[4]. Drugs. 2018 Dec;78(18):1931-1937.

[5]. Drugs. 2020 Feb;80(3):285-313.

Omacycline belongs to the tetracycline class of antibiotics. Omacycline is a tetracycline antibacterial drug. See also: omacycline (note moved to); omacycline tosylate (note moved to). Omacycline is the first intravenous and oral 9-aminomethylcycline to enter clinical development for the treatment of a variety of infectious diseases, including acute bacterial skin and soft tissue infections (ABSSSI), community-acquired bacterial pneumonia (CABP), and urinary tract infections (UTI). This study determined the in vitro activity of omacycline against a variety of Gram-positive clinical isolates, including methicillin-resistant Staphylococcus aureus (MRSA), vancomycin-resistant enterococci (VRE), group A and B β-hemolytic streptococci, penicillin-resistant Streptococcus pneumoniae (PRSP), and Haemophilus influenzae (H. influenzae). Omaliacycline showed MIC90 values of 1.0 μg/ml, 0.25 μg/ml, and 0.5 μg/ml against MRSA, VRE, and β-hemolytic streptococci, respectively, and MIC90 values of 0.25 μg/ml and 2.0 μg/ml against PRSP and Haemophilus influenzae, respectively. Omaliacycline is effective against pathogens exhibiting two main resistance mechanisms (ribosomal protection and active tetracycline efflux). The in vivo efficacy of omaliacycline was confirmed using a mouse intraperitoneal infection model. A single intravenous injection of omaliacycline was effective against Streptococcus pneumoniae, Escherichia coli, and Staphylococcus aureus, including strains carrying tet(M) and tet(K) efflux genes, as well as methicillin-resistant Staphylococcus aureus (MRSA) strains. The median effective dose (ED50) against Streptococcus pneumoniae ranged from 0.45 mg/kg to 3.39 mg/kg, against Staphylococcus aureus from 0.30 mg/kg to 1.74 mg/kg, and against Escherichia coli from 2.02 mg/kg. These results indicate that omalicycline has potent in vivo efficacy, including activity against strains containing common resistance determinants. In vitro studies have shown that omalicycline is active against a variety of Gram-positive bacteria and some Gram-negative pathogens, including strains containing resistance determinants, and that this activity translates into potent in vivo efficacy. [1]

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Omalicycline is a novel aminomethyltetracycline antibiotic currently being developed for oral and intravenous (IV) treatment of community-acquired bacterial infections. Omalicycline is characterized by the introduction of an aminomethyl substituent at the C9 position of the core six-membered ring. This modification enhances the antibacterial spectrum by overcoming known resistance to ribosomal protective proteins and efflux pump mechanisms that affect older generations of tetracyclines. In vitro studies have demonstrated that omalicycline is active against Gram-positive and Gram-negative aerobic and anaerobic bacteria, as well as atypical pathogens including Legionella and Chlamydia. Omalicycline can be administered orally or intravenously once daily, and its clinical tolerability and safety are comparable to those of commonly used antibiotics for treating severe community-acquired infections, especially given the declining efficacy of many antibiotics due to resistance. In studies of patients with complicated skin and soft tissue infections, including methicillin-resistant Staphylococcus aureus (MRSA) infections, omalicycline showed efficacy and tolerability comparable to linezolid. Ongoing and planned clinical studies are evaluating the efficacy of omalicycline as monotherapy for severe community-acquired bacterial infections, including acute bacterial skin and soft tissue infections (ABSSSI) and community-acquired bacterial pneumonia (CABP). This review summarizes the discovery, microbiological, non-clinical data, and existing clinical safety and efficacy data of omalicycline, referencing other contemporary tetracycline antibiotics. [2]

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Omacycline (Nuzyra®) is a novel aminomethylcycline antibiotic approved by the U.S. Food and Drug Administration (FDA) in 2018. It belongs to the tetracycline class of antimicrobial agents. It is used to treat community-acquired pneumonia and acute bacterial skin and soft tissue infections. The drug was developed and commercialized by Paratek Pharmaceuticals. It is a semi-synthetic compound derived from minocycline that can evade widely existing resistance mechanisms (such as efflux pumps and targeted protection) and has been shown to be effective against a variety of bacteria. [3]

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Paratek Pharmaceuticals is developing omacycline (NUZYRA™), a first-in-class oral active aminomethylcycline antimicrobial agent for the treatment of a variety of bacterial infections. The drug is available in intravenous and oral formulations and has broad-spectrum antimicrobial activity. It was recently approved in the United States for the treatment of community-acquired bacterial pneumonia (CABP) and acute bacterial skin and soft tissue infections (ABSSSI) in adults. This article summarizes the development process of omalicycline, which ultimately led to its first global approval for the treatment of CABP and ABSSSI. [4]

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Omalicycline (PTK 0796) is a novel semi-synthetic 9-aminomethylcycline antibiotic derived from minocycline. Its chemical name is (4S,4aS,5aR,12aS)-4,7-bis(dimethylamino)-9[((2,2-dimethylpropyl)amino]methyl]-3,10,12,12a-tetrahydroxy-1,11-dioxo-1,4,4a,5,5a,6,11,12a-octahydrotetraphenyl-2-carboxamide. [1]
Its development aims to overcome common tetracycline resistance mechanisms (ribosome protection and efflux pumps) and to be effective against a variety of pathogens, including multidrug-resistant strains. It is active. [1] At the time of publication, omalicycline was in clinical development for acute bacterial skin and skin structure infections (ABSSSI), community-acquired bacterial pneumonia (CABP), and urinary tract infections (UTI), and was available in both intravenous and oral formulations. [1] It exhibits potent in vitro activity against a variety of pathogens. The presence of resistant pathogens and its efficacy in lethal in vivo infection models support further clinical evaluation. [1]

C29H40N4O7

556.66

556.29

C, 62.57; H, 7.24; N, 10.07; O, 20.12

389139-89-3

Omadacycline tosylate;1075240-43-5;Omadacycline hydrochloride;1196800-39-1;Omadacycline-d9;2272886-41-4;Omadacycline mesylate;1196800-40-4; 389139-89-3

54697325

Light yellow to yellow solid powder

2.706

6

10

7

40

1140

4

O([H])[C@@]12C(=C(C(N([H])[H])=O)C([C@]([H])([C@]1([H])C([H])([H])[C@]1([H])C([H])([H])C3=C(C([H])=C(C([H])([H])N([H])C([H])([H])C(C([H])([H])[H])(C([H])([H])[H])C([H])([H])[H])C(=C3C(=C1C2=O)O[H])O[H])N(C([H])([H])[H])C([H])([H])[H])N(C([H])([H])[H])C([H])([H])[H])=O)O[H]

JEECQCWWSTZDCK-IQZGDKDPSA-N

InChI=1S/C29H40N4O7/c1-28(2,3)12-31-11-14-10-17(32(4)5)15-8-13-9-16-21(33(6)7)24(36)20(27(30)39)26(38)29(16,40)25(37)18(13)23(35)19(15)22(14)34/h10,13,16,21,31,34,36-37,40H,8-9,11-12H2,1-7H3,(H2,30,39)/t13-,16-,21-,29-/m0/s1

(4S,4aS,5aR,12aS)-4,7-bis(Dimethylamino)-9-(((2,2-dimethylpropyl)amino)methyl)- 3,10,12,12a- tetrahydroxy-1,11-dioxo-1,4,4a,5,5a,6,11,12a-octahydrotetracene-2- carboxamide

PTK-0796; PTK 0796; Omadacycline; Amadacycline; 389139-89-3; nuzyra; PTK0796; Nuzyra;Amadacyclin

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: Please store this product in a sealed and protected environment (e.g. under nitrogen), avoid exposure to moisture and light.

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

Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.

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Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)
*Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution.
Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)
Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil)
Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals).

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Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)]
*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.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)

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Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium)
Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose
Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals).

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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders

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Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

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