Table 2.

Quantification of the cellular uptake of studied inhibitors by H. pylori 26695 strain cells. The extracellular inhibitor concentration was determined by three detection methods: LC–MS, UV absorption spectra of the tested compounds, and inhibition of the target enzyme, as described in the text. The t-test was used to check for a significant difference in extracellular inhibitor concentration between supernatants incubated with and without H. pylori cells. The intracellular accumulation of each drug was determined using Eq. (1) or Eq. (5) as described in the text. Results of the t-test are marked as follows: ****p < 0.0001; ***p < 0.001; **p < 0.01, *p < 0.05; ns p > 0.05, not significant difference

Inhibitor	Starting inhibitor concentration [µM]	Method	Observation wavelength [nm]	Intracellular accumulation [µM]	Ki [µM]	t-test
Metronidazole	0.5	LC–MS	-	0.37 ± 0.01		****
Hadacidin	35	AdSS inhibition	-	4.9 ± 4.1	0.19 ± 0.02 vs. AdSSa	ns
Formycin A	350	UV absorptionc	305	22.2 ± 7.6	14.0 ± 1.7 vs. PNPb	*
	350	UV absorption	294	35.2 ± 7.1		**
	350	LC–MS	-	29.5 ± 5.3		*
	35	UV absorption	305	6.7 ± 0.6		***
	35	LC–MS	-	15.9 ± 0.5		****
Formycin B	350	LC–MS	-	7.1 ± 2.5	0.96 ± 0.08 vs. PNP	*
	350	UV absorption	279	3.0 ± 9.2		ns
	350	UV absorption	294	1.0 ± 7.4		ns
	350	PNP inhibition	-	20.2 ± 34.0		ns
	35	LC–MS	-	2.5 ± 0.5		**

^aFrom Bubić et al. (2018)

^bFrom Narczyk et al. (2018)

^cFrom Eq. (1), no correction for absorption of metabolites excreted to the medium by H. pylori was done