| Name | P glycoprotein |
|---|---|
| Synonyms | ABC20; MDR1; ABCB 1; ABCB1; ATP binding cassette sub family B member 1; CD243; CD243 antigen; CLCS… |
| Name | sodium azide |
|---|---|
| CAS | sodium azide |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 11745716 | Pavek P, Fendrich Z, Staud F, Malakova J, Brozmanova H, Laznicek M, Semecky V, Grundmann M, Palicka V: Influence of P-glycoprotein on the transplacental passage of cyclosporine. . J Pharm Sci. 2001 Oct;90(10):1583-92. Sodium azide, a mitochondrial respiratory inhibitor, was found to double the rate of cyclosporine, but not L-[(3) H]- passage across the placenta. |
3(0,0,0,3) | Details |
| 11288109 | Hamilton KO, Backstrom G, Yazdanian MA, Audus KL: P-glycoprotein efflux pump expression and activity in Calu-3 cells. J Pharm Sci. 2001 May;90(5):647-58. The metabolic inhibitor sodium azide decreased the efflux of Rh123 out of Calu-3 cells to the same degree as CsA, supporting inhibition of an active, efflux pathway. |
2(0,0,0,2) | Details |
| 10366541 | Diah SK, Smitherman PK, Townsend AJ, Morrow CS: Detoxification of 1-chloro-2,4-dinitrobenzene in MCF7 breast cancer cells expressing glutathione S-transferase P1-1 and/or multidrug resistance protein 1. Toxicol Appl Pharmacol. 1999 Jun 1;157(2):85-93. |
2(0,0,0,2) | Details |
| 15486199 | Loganzo F, Hari M, Annable T, Tan X, Morilla DB, Musto S, Zask A, Kaplan J, Minnick AA Jr, May MK, Ayral-Kaloustian S, Poruchynsky MS, Fojo T, Greenberger LM: Cells resistant to HTI-286 do not overexpress P-glycoprotein but have reduced drug accumulation and a point mutation in alpha-tubulin. Mol Cancer Ther. 2004 Oct;3(10):1319-27. It has excellent in vivo antitumor activity in human xenograft models, including tumors that express P-glycoprotein, and is in phase II clinical evaluation. Sodium azide treatment partially reversed low HTI-286 accumulation, suggesting involvement of an ATP-dependent drug pump. |
2(0,0,0,2) | Details |
| 9139856 | Lautier D, Bailly JD, Demur C, Herbert JM, Bousquet C, Laurent G: Altered intracellular distribution of daunorubicin in immature acute myeloid leukemia cells. Int J Cancer. 1997 Apr 10;71(2):292-9. Furthermore, PSC833, a potent P-gp blocker, had little effect on drug sequestration in CD34+ AML cells. |
2(0,0,0,2) | Details |
| 10856430 | Nielsen D, Maare C, Eriksen J, Litman T, Friche E, Skovsgaard T: Characterisation of multidrug-resistant Ehrlich ascites tumour cells selected in vivo for resistance to etoposide. Biochem Pharmacol. 2000 Aug 1;60(3):353-61. The multidrug resistance-associated protein (MRP) mRNA was increased 20-fold in EHR2/VP16 as compared with EHR2, whereas the expression of P-glycoprotein was unchanged. Deprivation of energy by addition of sodium azide increased the accumulation of both drugs to the level of sensitive cells. |
2(0,0,0,2) | Details |
| 7743893 | Lahmy S, Viallet P, Salmon JM: Is reduced accumulation of Hoechst 33342 in multidrug resistant cells related to P-glycoprotein activity?. Cytometry. 1995 Feb 1;19(2):126-33. Competition experiments with sodium azide, and vinblastine indicated that resistant cells did not differ in the number of possible binding sites for H342. |
2(0,0,0,2) | Details |
| 19881253 | Takano M, Otani Y, Tanda M, Kawami M, Nagai J, Yumoto R: Paclitaxel-resistance conferred by altered expression of efflux and influx transporters for paclitaxel in the human hepatoma cell line, HepG2. Drug Metab Pharmacokinet. 2009;24(5):418-27. The uptake of [(3) H] paclitaxel and rhodamine 123 increased by a P-gp inhibitor. |
2(0,0,0,2) | Details |
| 12047375 | Goda K, Nagy H, Mechetner E, Cianfriglia M, Szabo G Jr: Effects of ATP depletion and analogues on P-glycoprotein conformation in live cells. Eur J Biochem. 2002 Jun;269(11):2672-7. |
2(0,0,0,2) | Details |
| 11438421 | Valenzuela B, Nacher A, Casabo VG, Martin-Villodre A: The influence of active secretion processes on intestinal absorption of in the rat. Eur J Pharm Biopharm. 2001 Jul;52(1):31-7. was perfused in the small intestine of rat using a standard rat gut "in situ" preparation: (1) in inhibitor-free solution at seven different concentrations (0.15, 0.29, 1.20, 5.0, 9.0, 13.0 and 18.0mM); (2) at a 0.29mM concentration - thought to be close to the allometric dose in man - in the presence of a non-specific enzyme inhibitor, sodium azide (0.3, 3.0 and 6.0mM); and (3) at 0.29mM in the presence of a selective secretion inhibitor, (10.0 and 20.0mM). These results indicate that can act as a substrate of an intestinal secretory transport, which probably includes--at least in part--the enzyme P-glycoprotein, since has been shown to inhibit this enzyme by dose-dependent competition. |
1(0,0,0,1) | Details |
| 17604344 | Iwakiri T, Okumura M, Hidaka M, Kumagai Y, Ichihara E, Kawano Y, Arimori K: Inhibition of carrier-mediated uptake of epirubicin reduces cytotoxicity in primary culture of rat hepatocytes. J Appl Toxicol. 2008 Apr;28(3):329-36. Epirubicin, an antineoplastic drug, is considered to be taken up by tumor cells via a common carrier by facilitated diffusion and is then pumped out in an energy-dependent manner because epirubicin is a substrate for P-glycoprotein (P-gp). The uptake of epirubicin at a clinical concentration (7.5 x 10 (-7) M) was significantly reduced at 4 degrees C and significantly inhibited when pretreated with metabolic inhibitors (carbonyl p-trifluoromethoxyphenylhydrazone (FCCP), rotenone and sodium azide) by nearly 25%. |
1(0,0,0,1) | Details |
| 17215890 | Aurade R, Jayalakshmi SK, Sreeramulu K: Stimulatory effect of insecticides on partially purified P-glycoprotein ATPase from the resistant pest Helicoverpa armigera. Biochem Cell Biol. 2006 Dec;84(6):1045-50. Other inhibitors, such as EDTA, sodium azide, and resulted in only a 20% decrease in activity. |
2(0,0,0,2) | Details |
| 9186779 | Richardson DR: Mobilization of iron from neoplastic cells by some iron chelators is an energy-dependent process. Biochim Biophys Acta. 1997 May 16;1320(1):45-57. Interestingly, the metabolic inhibitors, 2,4-dinitrophenol, oligomycin, rotenone, and sodium azide, markedly decreased 59Fe mobilization mediated by PIH, but had either no effect or much less effect on 59Fe release by 311. Considering that an ATP-dependent process was involved in 59Fe release by PIH, further studies examined 4 widely used inhibitors of the multi-drug efflux pump P-glycoprotein (P-gp). |
1(0,0,0,1) | Details |
| 9165537 | Saitoh H, Fujisaki H, Aungst BJ, Miyazaki K: Restricted intestinal absorption of some beta-lactam antibiotics by an energy-dependent efflux system in rat intestine. Pharm Res. 1997 May;14(5):645-9. This energy-demanding efflux system was distinct from P-glycoprotein-mediated transport. Addition of sodium azide into an experimental buffer including significantly and selectively enhanced mucosal-to-serosal permeation of cephaloridine and cefoperazone. |
1(0,0,0,1) | Details |
| 12893836 | Dallas S, Zhu X, Baruchel S, Schlichter L, Bendayan R: Functional expression of the multidrug resistance protein 1 in microglia. J Pharmacol Exp Ther. 2003 Oct;307(1):282-90. Epub 2003 Jul 31. Vincristine accumulation by monolayers of MLS-9 cells increased significantly in the presence of several well established MRP1 inhibitors (MK571, sulfinpyrazone, probenecid, and indomethacin), protease inhibitors, or the ATPase inhibitor sodium azide. |
1(0,0,0,1) | Details |
| 9030742 | Draper MP, Martell RL, Levy SB: Active efflux of the free acid form of the fluorescent dye 2',7'-bis (2-carboxyethyl)-5 (6)-carboxyfluorescein in multidrug-resistance-protein-overexpressing murine and human leukemia cells. Eur J Biochem. 1997 Jan 15;243(1-2):219-24. In contrast, less altered accumulation was seen in the P-glycoprotein (P-gp)-overexpressing cell lines. The decreased drug accumulation was reversed by the energy inhibitors sodium azide/2-deoxyglucose and by the vinca alkaloid, vincristine, but not by the chemotherapeutic agents, etoposide and adriamycin. |
1(0,0,0,1) | Details |
| 7945406 | Versantvoort CH, Broxterman HJ, Lankelma J, Feller N, Pinedo HM: Competitive inhibition by and ATP dependence of daunorubicin transport in intact MRP overexpressing human small cell lung cancer cells. Biochem Pharmacol. 1994 Sep 15;48(6):1129-36. In several multidrug resistant tumor cell lines without overexpression of P-glycoprotein (non-Pgp MDR), a decreased accumulation of drugs has been shown to contribute to resistance. Marked inhibition of DNR transport activity in intact GLC4/ADR cells was found when cellular ATP concentration was decreased below 2 mM by sodium azide or 2-deoxy- |
1(0,0,0,1) | Details |
| 10470369 | Hall JG, Cory AH, Cory JG: Lack of competition of substrates for P-glycoprotein in MCF-7 breast cancer cells overexpressing MDR1. Adv Enzyme Regul. 1999;39:113-28. On short-term incubation, 2-deoxyglucose lowers the NTP levels to a greater extent than sodium azide, showing the importance of glycolysis in the MCF-7 cell lines. 6. |
1(0,0,0,1) | Details |
| 16574353 | Valenzuela B, Lopez-Pintor E, Perez-Ruixo JJ, Nacher A, Martin-Villodre A, Casabo VG: Modelling intestinal absorption of in rats. Int J Pharm. 2006 May 11;314(1):21-30. Epub 2006 Mar 30. at concentration of 0.29 mM was administered in presence of (10 and 20 mM), grapefruit juice and sodium azide (NaN3) (0.3, 3 and 6 mM). The validated model suggested instantaneous equilibrium between concentrations in lumen and enterocyte, and the absorption was best described by a simultaneous passive diffusion (ka = 0.636 h (-1)) and active absorption (VMax = 0.726 mM/h, Km = 0.540 mM) processes from intestinal lumen to enterocyte, together with an active capacity-limited P-gp efflux (V'max = 0.678 mM/h, K'm = 0.357 mM) from enterocyte to intestinal lumen. |
1(0,0,0,1) | Details |
| 16595934 | Kawazu K, Oshita A, Nakamura T, Nakashima M, Ichikawa N, Sasaki H: Transport of acebutolol through rabbit corneal epithelium. Biol Pharm Bull. 2006 Apr;29(4):846-9. Thus, it was suggested that acebutolol was actively secreted via P-glycoprotein in a corneal epithelium. Sodium azide, and cyclosporin A enhanced the transcellular permeability of acebutolol in the A-to-B direction. |
1(0,0,0,1) | Details |
| 10202553 | Bogush TA, Smirnova GB, Bogush EA, Robert J: [A new method for the intravital assessment of the functional activity of the membrane transporters performing the efflux of antitumor preparations from the cells of solid tumor specimens]. Antibiot Khimioter. 1999;44(2):19-24. To assess just the intracellular content of Dox and to estimate the transporter functional activity, investigation of the influence of membrane transporter inhibitors such as (P-gp inhibitor) and sodium azide (inhibitor of all the energy-dependent ABC transporters) on the drug fluorescence decrease in the incubation medium is stipulated. To assess just the intracellular content of Dox and to estimate the transporter functional activity, investigation of the influence of membrane transporter inhibitors such as (P-gp inhibitor) and sodium azide (inhibitor of all the energy-dependent ABC transporters) on the drug fluorescence decrease in the incubation medium is stipulated. |
1(0,0,0,1) | Details |
| 10211547 | Lam W, Chan H, Yang M, Cheng S, Fong W: Synergism of energy starvation and dextran-conjugated doxorubicin in the killing of multidrug-resistant KB carcinoma cells. Anticancer Drugs. 1999 Feb;10(2):171-8. Our results suggest that energy starvation, in addition to increasing cellular retention of P-gp substrates, may affect cellular fate of conjugated drugs with a possible enhancing effect in cancer cell killing. |
1(0,0,0,1) | Details |
| 8043436 | Jiang XR, Macey MG, Collins PW, Newland AC: Characterization and modulation of drug transport kinetics in K562 c1.6 daunorubicin-resistant cell line. Br J Haematol. 1994 Mar;86(3):547-54. An increase in DAU accumulation, intracellular SL and the time to reach 90% saturation level (SL90), and a decrease in DAU efflux in the resistant but not the sensitive cells were found in response to ATP depletion by sodium azide. K562 c1.6/DAU resistant cells displayed high levels of P-glycoprotein and a high level of multidrug resistance against several antitumour drugs. |
1(0,0,0,1) | Details |
| 8937472 | Slapak CA, Martell RL, Terashima M, Levy SB: Increased efflux of vincristine, but not of daunorubicin, associated with the murine multidrug resistance protein (MRP). Biochem Pharmacol. 1996 Nov 22;52(10):1569-76. Only PC-V160, selected for high level resistance, demonstrated concomitant overexpression of the P-glycoprotein. |
1(0,0,0,1) | Details |
| 7671247 | Lorico A, Rappa G, Srimatkandada S, Catapano CV, Fernandes DJ, Germino JF, Sartorelli AC: Increased rate of -dependent etoposide (VP-16) efflux in a murine leukemia cell line overexpressing the multidrug resistance-associated protein (MRP) gene. Cancer Res. 1995 Oct 1;55(19):4352-60. In the presence of the inhibitors of energy metabolism, sodium azide and deoxyglucose, the efflux of VP-16 was markedly inhibited; readdition of restored the original efflux rate. |
0(0,0,0,0) | Details |
| 16010862 | Zhou S, Li Y, Kestell P, Schafer P, Chan E, Paxton JW: Transport of thalidomide by the human intestinal caco-2 monolayers. Eur J Drug Metab Pharmacokinet. 2005 Jan-Jun;30(1-2):49-61. Additional data indicated that transport of thalidomide is energy-dependent, as it was significantly (P < 0.05) inhibited by the ATP inhibitors, sodium azide and 2,4-dinitrophenol. |
0(0,0,0,0) | Details |
| 14728974 | Brunet JL, Maresca M, Fantini J, Belzunces LP: Human intestinal absorption of imidacloprid with Caco-2 cells as enterocyte model. Toxicol Appl Pharmacol. 2004 Jan 1;194(1):1-9. Decrease of uptake with sodium-azide or after cell surface trypsin (Ti) treatment suggested the involvement of a trypsin-sensitive ATP-dependent transporter. |
0(0,0,0,0) | Details |
| 10930538 | Yang CH, Schneider E, Kuo ML, Volk EL, Rocchi E, Chen YC: BCRP/MXR/ABCP expression in topotecan-resistant human breast carcinoma cells. Biochem Pharmacol. 2000 Sep 15;60(6):831-7. Topotecan efflux was increased in MCF7/TPT300 cells compared with MCF7/WT cells, and this increase was reversed upon ATP depletion by sodium azide, suggesting an energy-dependent drug efflux mechanism. |
0(0,0,0,0) | Details |
| 9972316 | Podsiadlowski L, Matha V, Vilcinskas A: Detection of a P-glycoprotein related pump in Chironomus larvae and its inhibition by and cyclosporin A. Comp Biochem Physiol B Biochem Mol Biol. 1998 Dec;121(4):443-50. This increase was unaffected by inhibitors of other membrane ATPases (sodium azide, EGTA, ouabain), but sensitive to vanadate, cyclosporin A and which inhibit mammalian P-glycoprotein mediated ATP-consumption. |
88(1,1,1,8) | Details |
| 12112443 | Bendayan R, Lee G, Bendayan M: Functional expression and localization of P-glycoprotein at the blood brain barrier. Microsc Res Tech. 2002 Jun 1;57(5):365-80. In addition, results from functional studies show that the accumulation of the P-glycoprotein substrate by RBE4 monolayer cells is significantly enhanced in the presence of standard P-glycoprotein inhibitors cyclosporin A, PSC 833), protease inhibitors (saquinavir, ritonavir, indinavir), and the metabolic inhibitor, sodium azide. |
39(0,1,1,9) | Details |
| 15180339 | Ronaldson PT, Lee G, Dallas S, Bendayan R: Involvement of P-glycoprotein in the transport of saquinavir and indinavir in rat brain microvessel endothelial and microglia cell lines. Pharm Res. 2004 May;21(5):811-8. Cellular accumulation of [14C] saquinavir and [3H] indinavir by RBE4, MLS-9, and CHRC5 monolayers was significantly enhanced in the presence of P-gp inhibitors, HIV-1 protease inhibitors, the ATPase inhibitor sodium azide, and the ATP depleting agent 2',4'-dinitrophenol respectively. [14C] Saquinavir and [3H] indinavir efflux from both cell systems was rapid and significantly reduced in the presence of PSC833. |
36(0,1,1,6) | Details |
| 11561081 | Lee G, Schlichter L, Bendayan M, Bendayan R: Functional expression of P-glycoprotein in rat brain microglia. J Pharmacol Exp Ther. 2001 Oct;299(1):204-12. Immunocytochemical analysis with the monoclonal antibodies C219, MRK16, and MAB-448 labeled P-gp protein along the plasma membrane and nuclear envelope of MLS-9 cells. [3H] accumulation by monolayers of MLS-9 cells was significantly enhanced in the presence of any of several P-gp inhibitors cyclosporin A, quinidine, PSC 833), protease inhibitors (i.e., saquinavir, indinavir, and ritonavir), and sodium azide, an ATPase inhibitor. |
36(0,1,1,6) | Details |
| 14999725 | Shono Y, Nishihara H, Matsuda Y, Furukawa S, Okada N, Fujita T, Yamamoto A: Modulation of intestinal P-glycoprotein function by cremophor EL and other surfactants by an in vitro diffusion chamber method using the isolated rat intestinal membranes. J Pharm Sci. 2004 Apr;93(4):877-85. The Jsm/Jms ratio of rhodamine123 decreased in the presence of 0.3 mM and 10 mM sodium azide (NaN3) + 1 mM (NaF), confirming that rhodamine123 might be secreted from the intestinal tissue into the lumen by a P-gp-mediated efflux system. |
86(1,1,1,6) | Details |
| 7646548 | Nielsen D, Maare C, Skovsgaard T: Influx of daunorubicin in multidrug resistant Ehrlich ascites tumour cells: correlation to expression of P-glycoprotein and efflux. Biochem Pharmacol. 1995 Aug 8;50(4):443-50. |
7(0,0,0,7) | Details |
| 12626638 | Pavek P, Staud F, Fendrich Z, Sklenarova H, Libra A, Novotna M, Kopecky M, Nobilis M, Semecky V: Examination of the functional activity of P-glycoprotein in the rat placental barrier using rhodamine 123. J Pharmacol Exp Ther. 2003 Jun;305(3):1239-50. Epub 2003 Mar 6. |
7(0,0,0,7) | Details |
| 11070177 | Ushigome F, Takanaga H, Matsuo H, Yanai S, Tsukimori K, Nakano H, Uchiumi T, Nakamura T, Kuwano M, Ohtani H, Sawada Y: Human placental transport of vinblastine, vincristine, and contribution of P-glycoprotein. Eur J Pharmacol. 2000 Nov 10;408(1):1-10. The uptake of [(3) H] vinblastine and [(3) H] vincristine into BeWo cells was increased in the presence of a metabolic inhibitor, sodium azide. |
6(0,0,0,6) | Details |
| 10215691 | Henthorn TK, Liu Y, Mahapatro M, Ng KY: Active transport of by the blood-brain barrier. J Pharmacol Exp Ther. 1999 May;289(2):1084-9. uptake was also significantly inhibited by either 4 degrees C or sodium azide/2-deoxyglucose, suggesting that carrier-mediated uptake of was an active process. was also tested to determine whether it might be a substrate of the endogenous blood-brain barrier efflux transport system, P-glycoprotein (P-gp). |
6(0,0,0,6) | Details |
| 16221533 | Lecoeur S, Videmann B, Mazallon M: Effect of organophosphate pesticide diazinon on expression and activity of intestinal P-glycoprotein. Toxicol Lett. 2006 Mar 1;161(3):200-9. Epub 2005 Oct 10. The efflux rate significantly decreased in the presence of metabolic inhibitors sodium azide and 2-deoxy- P-gp inhibitors cyclosporin A and valspodar, but not in the presence of MRPs inhibitor MK571. |
5(0,0,0,5) | Details |
| 7949184 | Slapak CA, Mizunuma N, Kufe DW: Expression of the multidrug resistance associated protein and P-glycoprotein in doxorubicin-selected human myeloid leukemia cells. Blood. 1994 Nov 1;84(9):3113-21. Treatment with sodium azide/2-deoxyglucose, 2,4-dinitrophenol, or monensin, but not abolished the vesicular accumulation. |
5(0,0,0,5) | Details |
| 12956939 | Zhang L, Liu XD, Xie L, Wang GJ: P-glycoprotein restricted transport of nimodipine across blood-brain barrier. Acta Pharmacol Sin. 2003 Sep;24(9):903-6. The steady-state uptake was also significantly increased (P <0.01) when cellular ATP was depleted by treatment with sodium azide. |
5(0,0,0,5) | Details |
| 20190417 | Ishikawa Y, Nagai J, Okada Y, Sato K, Yumoto R, Takano M: Function and expression of ATP-binding cassette transporters in cultured human Y79 retinoblastoma cells. Biol Pharm Bull. 2010;33(3):504-11. The aim of this study was to reveal the expression and function of P-glycoprotein and multidrug resistance-associated proteins (MRP), members of the ATP-binding cassette (ABC) superfamily of drug transporters, in cultured human Y79 retinoblastoma cells. The accumulation of doxorubicin was increased in the presence of metabolic inhibitors (10 mM 2-deoxyglucose and 5 mM sodium azide). |
4(0,0,0,4) | Details |
| 7902705 | Garrigos M, Belehradek J Jr, Mir LM, Orlowski S: Absence of cooperativity for MgATP and effects on the ATPase activity of P-glycoprotein containing membrane vesicles. Biochem Biophys Res Commun. 1993 Nov 15;196(3):1034-41. |
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| 10393043 | Kawazu K, Yamada K, Nakamura M, Ota A: Characterization of cyclosporin A transport in cultured rabbit corneal epithelial cells: P-glycoprotein transport activity and binding to cyclophilin. Invest Ophthalmol Vis Sci. 1999 Jul;40(8):1738-44. |
4(0,0,0,4) | Details |
| 10368660 | Candussio L, Decorti G, Crivellato E, Rosati AM, Traversa U, Klugmann FB: Transport of doxorubicin in mast cell granules and the effect of the antagonist Anticancer Res. 1999 Mar-Apr;19(2A):1101-8. P-glycoprotein has been identified in mast cells stabilized in culture as well as in rat peritoneal mast cells, and is primarily concentrated on the granular membrane. Similar results were obtained with the metabolic inhibitors metavanadate, N-ethylmaleimide, and sodium azide, whereas ouabain, an inhibitor of - ATPase, was without effect. |
4(0,0,0,4) | Details |
| 11724763 | Florea BI, van der Sandt IC, Schrier SM, Kooiman K, Deryckere K, de Boer AG, Junginger HE, Borchard G: Evidence of P-glycoprotein mediated apical to basolateral transport of flunisolide in human broncho-tracheal epithelial cells (Calu-3). Br J Pharmacol. 2001 Dec;134(7):1555-63. Non-specific inhibition of cellular metabolism at low temperature (4 degrees C) or by 2-deoxy- (2-d- and sodium azide (NaN (3)) abolished the polarized transport. |
4(0,0,0,4) | Details |
| 9260877 | Cleary I, Doherty G, Moran E, Clynes M: The multidrug-resistant human lung tumour cell line, DLKP-A10, expresses novel drug accumulation and sequestration systems. Biochem Pharmacol. 1997 May 15;53(10):1493-502. Drug accumulation studies with the anticancer agents adriamycin and vincristine were carried out on the MDR variant of the human lung cell lines DLKP, DLKP-A10 which overexpresses the MDR associated P-glycoprotein efflux pump. Metabolic inhibition by antimycin A (but not sodium azide or 2-deoxy- resulted in complete restoration of drug accumulation suggesting the presence of an alternative energy dependent transport mechanism. |
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