Nocardicin A

Nocardicin A inhibits the β-lactam-supersensitive Escherichia coli Es-11 mutant strain with an MIC of 0.4 mcg/mL, which is 1000-fold lower than that of the parental Escherichia coli strain (MIC = 400 mcg/mL)^[2].
Nocardicin A (25 mcg/mL; overnight) converts Pseudomonas aeruginosa NCTC 10490 to protoplasts/spheroplasts after overnight incubation on agar containing 20% sucrose^[2].
Nocardicin A inhibits Pseudomonas aeruginosa, Proteus spp., Serratia marcescens, and Escherichia coli isolates in A-No.3/A-No.5 medium with MICs of 3.13-200 μg/mL^[3].
Nocardicin A exhibits higher MICs against Pseudomonas aeruginosa strains 191, 195, 201, and 161 and Proteus mirabilis strains 60, 100, and 105 in HI agar (> 800 μg/mL and 100-200 μg/mL, respectively), but lower MICs in A-No.3/A-No.5 agar (12.5-800 μg/mL and 6.25-12.5 μg/mL, respectively)^[3].
Nocardicin A potently inhibits B. thiaminolyticus IFO 3115 with an MIC of 0.78 μg/mL^[4].
Nocardicin A (1 mg/mL; 37°C overnight) activity against P. aeruginosa IFO 3080 is significantly antagonized by Glycine (HY-Y0966), D-Alanine (HY-41700), and D-Leucine (HY-Y0378), and partially antagonized by L-Alanine (HY-N0229) and L-Leucine (HY-N0486)^[4].
Nocardicin A is highly stable to the tested β-lactamases, with relative hydrolysis rates ranging from <0.01-6.55^[4].
Nocardicin A exhibits no β-lactamase inhibitory activity against the tested penicillinases and cephalosporinases (I₅₀ > 100 μg/mL)^[4].
Nocardicin A (100-1000 μg/mL; added after 2.5 h, with growth monitored until 7 h) exhibits the strongest lytic activity against P. aeruginosa IFO 3080 among the tested compounds, although it does not cause lysis at its MIC concentration^[4].
Nocardicin A (up to 100 μg/mL) binds PBP 1B but not PBP 1A in P. aeruginosa IFO 3080^[4].
Nocardicin A (incubated for 18 h) inhibits E. coli W-7, KN126, SP6, and SP61, with MIC ranging from 24-43 µM^[6].
Nocardicin A (40-160 µM) alone produces a slow bactericidal/lytic effect on E. coli W-7 at 40-80 µM, and a more rapid lytic response at 160 µM^[6].
Nocardicin A (40 µM) combined with Mecillinam (HY-A0269) (3 µM) rapidly induces lysis of E. coli W-7 and inhibits peptidoglycan synthesis^[6].
Nocardicin A (approximately 20 µM) and Mecillinam (0.1 µM) synergistically trigger lysis of E. coli W-7 and KN126, consistent with their respective MICs^[6].
Nocardicin A (40 µM) combined with Mecillinam (3 µM) induces lysis in E. coli KN126 and SP61 with normal PBP2 function, but does not induce lysis in the PBP2-deficient SP6^[6].
Nocardicin A combined with Amoxicillin (HY-B0467A) (4 µM) induces Mecillinam-like lysis in E. coli W-7, indicating that Mecillinam is not absolutely required as a PBP2 modulator^[6].
Nocardicin A (1 μg/mL; 18 h) in combination with Nva-Ala (P) exhibits a synergistic effect against Pseudomonas aeruginosa 511030, with an FICI of 0.25^[7].
Nocardicin A (3.6 μg/mL; 18 h) combined with Nva-Ala (P) exhibits the most pronounced synergy against Pseudomonas aeruginosa (20 isolates; mean FICI 0.24), and shows broader synergy in P. mirabilis, indole-positive Proteus spp., and S. marcescens^[7].
Nocardicin A (2 μg/mL; 2 h) combined with Nva-Ala (P) causes synergistic lysis of uridine-prelabeled Pseudomonas aeruginosa 511030, with a FICI of 0.18^[7].
Nocardicin A exhibits moderate anti-pseudomonal activity in vitro (MIC = 32 mg/L; MBC = 256 mg/L), shows partial inhibitory synergy with Carbenicillin (HY-B0525A), but has no bactericidal synergy against Ps. aeruginosa 30^[8].

Nocardicin A (20 h-3 days) exhibits moderate activity against Gram-negative bacteria, including Proteus vulgaris IAM-1025 and Shigella sonnei I EW-33 (MIC = 3.13 mcg/mL) as well as Pseudomonas aeruginosa IAM-1095 (MIC = 400 mcg/mL), and is inactive against Staphylococcus aureus FDA 209P, Mycobacterium phlei, fungi, or Candida albicans (MIC >800 to >1,600 mcg/mL)^[2].

Nocardicin A (5-20 μg/mL; 2 h) does not affect directed or random migration of human PMNs at 10 and 5 μg/mL, but impairs motility in the under-agarose migration assay at 20 μg/mL^[8].

Nocardicin A (0.1-10 μg/mL; 30 min) increases the intracellular killing of Ps. aeruginosa 30 by human PMNs^[8].