Macrolide
Midecamycin is a 16-membered macrolide antibiotic. Similar to classical macrolides (e.g., erythromycin, tylosin), its known mechanism of action is to bind to the peptidyltransferase center of the 50S subunit of the bacterial ribosome, thereby inhibiting bacterial protein synthesis.

Most strains of Haemophilus, Listeria, and staphylococci are inhibited by midecamycin at concentrations below 3.1 μg/mL[1]. Midecamycin is a macrolide with 16 members. A novel macrolide antibiotic called midecamycin is made by Streptomyces mycarofaciens[2].

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Midecamycin was tested against a range of gram-positive and gram-negative bacteria. It inhibited most streptococci, staphylococci, Haemophilus influenzae, and Listeria monocytogenes at concentrations of ≤ 3.1 μg/mL. Specifically, against Streptococcus pneumoniae, the MIC90 was 0.2 μg/mL. It was active against Campylobacter jejuni with an MIC of 3.1 μg/mL.
Midecamycin was less active than erythromycin in vitro, typically by a factor of two- to fourfold against most isolates of staphylococci, streptococci, H. influenzae, and S. pneumoniae.
It failed to inhibit erythromycin-resistant isolates of staphylococci and Streptococcus faecalis.
MICs were only slightly affected by increasing the inoculum size from 10³ to 10⁷ CFU when testing Staphylococcus aureus or Staphylococcus epidermidis (e.g., MICs changed from 0.1/0.8 μg/mL to 0.2/0.8-1.6 μg/mL). However, the minimal bactericidal concentrations (MBCs) increased substantially, from 1.6 and 3.1 μg/mL at 10³ CFU to 100 and >100 μg/mL at 10⁷ CFU.
It had poor activity against Bacteroides fragilis (MIC90 25 μg/mL) and no significant activity against Enterobacteriaceae or Pseudomonas spp. (MICs >100 μg/mL).

Minimal Inhibitory Concentration (MIC) Determination: For staphylococci and gram-negative bacteria, MICs were determined using Mueller-Hinton agar by the spot inoculum method with an inoculum of 10⁵ CFU. For streptococci and Listeria spp., MICs were determined on brain-heart infusion agar containing 5% sheep erythrocytes. The MIC was the lowest concentration inhibiting visible growth.
Minimal Bactericidal Concentration (MBC) Determination: MBCs were determined in Mueller-Hinton broth with an inoculum of 10⁵ CFU. From clear tubes, 0.1 ml was plated onto sheep blood agar plates. The MBC was the concentration at which no growth was observed on the agar plates after incubation.[1]

Absorption, Distribution and Excretion
Midecamycin is rapidly and almost completely absorbed after oral administration. It is primarily absorbed in the alkaline intestinal environment. This rapid absorption is attributed to its lipid solubility, allowing it to penetrate well into tissues, particularly bronchial secretions, prostate tissue, middle ear effusion, and bone tissue. A tissue/serum concentration ratio greater than 1 indicates that the product has a short residence time in plasma. After oral administration of 600 mg of midecamycin, the peak serum concentration is 0.8 mg/L, reached 1 hour after administration. This concentration decreases significantly after 4–6 hours. The primary route of excretion for midecamycin is the liver, followed by the kidneys, but renal excretion is minimal. Approximately 3.3% of the administered dose is present in urine 6 hours after administration. The apparent volume of distribution of midecamycin is reported to be 7.7 L/kg. Renal clearance of midecamycin is low. Metabolism/Metabolites Midecamycin undergoes extensive biotransformation in the liver, and its metabolites exhibit little to no antibacterial activity. The main metabolite is formed by 14-hydroxylation and can also be detected in urine.
Biological Half-Life
The half-life of midecamycin is longer than that of first-generation macrolide antibiotics. The reported half-life after intravenous administration is 54 minutes.

Protein Binding
Midcamycin binds very little to plasma proteins; therefore, the bound form of the drug accounts for approximately 15% of the administered dose. Midcamycin acetate has a higher protein binding rate.

[1]. Neu HC. In vitro activity of midecamycin, a new macrolide antibiotic. Antimicrob Agents Chemother. 1983 Sep;24(3):443-4.

[2]. Cloning and characterization of genes encoded in dTDP-D-mycaminose biosynthetic pathway from amidecamycin-producing strain, Streptomyces mycarofaciens. Acta Biochim Biophys Sin (Shanghai). 2007 Mar;39(3):187-93.

Midcamycin is an organic molecular entity. It is a naturally occurring 16-membered macrolide antibiotic, belonging to the acetoxy-substituted macrolide class. In this molecule, the acetoxy group substitutes for the 9th position of the 16-membered ring and the 4th position of the terminal sugar. Until 2017, midcamycin was listed in Health Canada's list of approved antimicrobial active pharmaceutical ingredients. Drug Indications Midcamycin has been used to treat oral, upper and lower respiratory tract infections, as well as skin and soft tissue infections. Its use alone is primarily in Europe and Japan. Mechanism of Action As a macrolide antibiotic, midcamycin exerts its effect by inhibiting bacterial protein synthesis. More specifically, midcamycin inhibits bacterial growth by targeting the 50S ribosomal subunit, preventing peptide bond formation and translocation during protein synthesis. Mutations in the 50S RNA prevent the binding of midcamycin. Midcamycin is a broad-spectrum antibiotic and therefore can interact with a wide variety of bacteria. Midcamycin is a 16-membered macrolide antibiotic produced by Streptomyces mycarofaciens. Its structure consists of a polyketide-derived lactone ring (aglycone) with two deoxyhexoses—macaminoose and macarose—sequentially linked to it. This study cloned and identified two gene subclusters from S. mycarofaciens involved in the biosynthesis of the first deoxysugar in midcamycin—dTDP-D-macaminoose—and its transfer to the aglycone. The identified genes include midA (dTDP-glucose synthase), midB (dTDP-glucose-4,6-dehydratase), midC (aminotransferase), midK (methyltransferase), midI (glycosyltransferase), and midH (auxiliary protein). The biosynthetic pathway of dTDP-D-macaminoses begins with glucose-1-phosphate, proceeding via dTDP-glucose and... dTDP-4-keto-6-deoxyglucose, with subsequent steps catalyzed by the products of midB, midC, and midK. The midI gene product is believed to be responsible for linking mycoamine to the midcamycin lactone ring. The midH gene product may serve as a cofactor for the highly efficient glycosyltransferase activity of MidI, similar to the desVIII/desVII gene pair in Streptomyces venezulatus and the tylMIII/tylMII gene pair in Streptomyces freundii. The gene structure shows that the polyketide synthase (PKS) gene is clustered in the center, flanked by deoxyglucose biosynthetic genes.

C41H67NO15

813.9684

813.451

C, 60.50; H, 8.30; N, 1.72; O, 29.48

35457-80-8

55881-07-7 (acetate);35457-80-8;

5282169

White to off-white solid powder

1.2±0.1 g/cm3

874.0±65.0 °C at 760 mmHg

155℃ -156℃

482.4±34.3 °C

0.0±0.6 mmHg at 25°C

1.536

3.53

3

16

14

57

1360

16

O([C@]1([H])C([H])([H])C(C([H])([H])[H])([C@]([H])(C([H])(C([H])([H])[H])O1)OC(C([H])([H])C([H])([H])[H])=O)O[H])[C@]1([H])C([H])(C([H])([H])[H])O[C@]([H])(C([H])(C1([H])N(C([H])([H])[H])C([H])([H])[H])O[H])O[C@]1([H])[C@]([H])([C@@]([H])(C([H])([H])C(=O)O[C@]([H])(C([H])([H])[H])C([H])([H])C([H])=C([H])C([H])=C([H])[C@@]([H])([C@]([H])(C([H])([H])[H])C([H])([H])[C@]1([H])C([H])([H])C([H])=O)O[H])OC(C([H])([H])C([H])([H])[H])=O)OC([H])([H])[H] |c:83,87|

DMUAPQTXSSNEDD-QALJCMCCSA-N

InChI=1S/C41H67NO15/c1-11-30(45)54-29-21-32(47)51-24(4)16-14-13-15-17-28(44)23(3)20-27(18-19-43)37(38(29)50-10)57-40-35(48)34(42(8)9)36(25(5)53-40)56-33-22-41(7,49)39(26(6)52-33)55-31(46)12-2/h13-15,17,19,23-29,33-40,44,48-49H,11-12,16,18,20-22H2,1-10H3/b14-13+,17-15+/t23-,24-,25-,26+,27+,28+,29-,33+,34-,35-,36-,37+,38+,39+,40+,41-/m1/s1

7-(Formylmethyl)-4,10-dihydroxy-5-methoxy-9,16-dimethyl-2-oxooxacyclohexadeca-11,13-dien-6-yl 3,6-dideoxy-4-O-(2,6-dideoxy-3-C-methyl-alpha-L-ribo-hexopyranosyl)-3-(dimethylamino)-beta-D-glucopyranoside 4',4''-dipropionate (ester)

SF 837; SF-837; SF837;

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 : 36~100 mg/mL ( 44.23~122.85 mM )
Ethanol : ~100 mg/mL

Solubility in Formulation 1: ≥ 2.25 mg/mL (2.76 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 22.5 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: ≥ 2.25 mg/mL (2.76 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 22.5 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: ≥ 2.25 mg/mL (2.76 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 22.5 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: ≥ 2.25 mg/mL (2.76 mM)

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