0.20 ± 0.03 mM V max = 0.70 ± 0.05 nmol/mg protein/min
[132]
|
|
hMATE2‐K
|
K m = 0.20 ± 0.03 mM V max = 3.0 ± 0.2 nmol/mg protein/min
|
[132]
|
|
(R,R)‐Fenoterol
|
MATE1
|
K m = 111.3 ± 16.3 μM V max = 2091.3 ± 133.7 pmol/mg protein/min
|
[41]
|
|
MATE2‐K
|
K m = 76.4 ± 4.1 μM V max = 728.6 ± 92.9 pmol/mg protein/min
|
[41]
|
|
(S,S)‐Fenoterol
|
MATE1
|
K m = 103.5 ± 18.0 μM V max = 1822.3 ± 360.6 pmol/mg protein/min
|
[41]
|
|
MATE2‐K
|
K m = 69.5 ± 1.1 μM V max = 511.7 ± 47.0 pmol/mg protein/min
|
[41]
|
|
(R,R)‐Formoterol
|
MATE1
|
K m = 231.5 ± 114.7 μM V max = 301.5 ± 152.3 pmol/mg protein/min
|
[41]
|
|
MATE2‐K
|
K m = 181.7 ± 158.1 μM V max = 77.6 ± 38.5 pmol/mg protein/min
|
[41]
|
|
(S,S)‐Formoterol
|
MATE1
|
K m = 343.8 ± 321.0 μM V max = 447.3 ± 363.4 pmol/mg protein/min
|
[41]
|
|
MATE2‐K
|
K m = 35.7 ± 12.5 μM V max = 33.7 ± 6.1 pmol/mg protein/min
|
[41]
|
|
Ganciclovir
|
hMATE1
|
K m = 5.12 ± 0.27 mM V max = 2.12 ± 0.25 nmol/mg protein/2 min
|
[27]
|
|
hMATE2‐K
|
K m = 4.28 ± 0.61 mM V max = 1.61 ± 0.27 nmol/mg protein/2 min
|
[27]
|
|
Ipratropium
|
MATE1
|
K m = 44.8 ± 2.9 μM V max = 3342.7 ± 183.6 pmol/mg protein/min
|
[44]
|
|
MATE2‐K
|
K m = 95.7 ± 7.5 μM V max = 2153.1 ± 219.3 pmol/mg protein/min
|
[44]
|
|
Metformin
|
hMATE1
|
K m = 0.78 ± 0.10 mM V max = 4.46 ± 0.59 nmol/mg 3 protein/2 min
|
[6]
|
|
K m = 228 ± 15.3 μM V max = 4.5 ± 0.19 nmol/min/mg protein
|
[133]
|
|
K m = 336 ± 202 μM
|
[59]
|
|
hMATE2‐K
|
K m = 1.05 ± 0.29 mM
|
[6]
|
|
K m = 1.98 ± 0.48 mM V max = 1.69 ± 0.34 nmol/mg protein/2 min
|
[27]
|
|
K m = 819 ± 69.5 μM V max = 7.1 ± 0.24 nmol/mg protein/min
|
[133]
|
|
cMATE1
|
K m = 340 ± 29.4 μM V max = 5.9 ± 0.34 nmol/mg protein/min
|
[133]
|
|
cMATE2‐K
|
K m = 1566 ± 407 μM V max = 15.9 ± 1.8 nmol/mg protein/min
|
[133]
|
|
Nadolol
|
MATE1
|
K m = 531 ± 170 μM
|
[42]
|
|
MATE‐2K
|
K m = 372 ± 84 μM
|
[42]
|
|
Procainamide
|
hMATE1
|
K m = 1.23 ± 0.03 mM V max = 7.56 ± 1.70 nmol/mg protein/2 min
|
[27]
|
|
hMATE2‐K
|
K m = 1.58 ± 0.04 mM V max = 6.77 ± 0.94 nmol/mg protein/2 min
|
[27]
|
|
Topotecan
|
hMATE1
|
K m = 0.07 ± 0.02 mM V max = 0.42 ± 0.13 nmol/mg protein/2 min
|
[27]
|
|
hMATE2‐K
|
K m = 0.06 ± 0.01 mM V max = 0.26 ± 0.02 nmol/mg protein/2 min
|
[27]
|
|
Trospium
|
MATE1
|
K m = 15.4 ± 2.4 μM V max = 1082.6 ± 142.7 pmol/mg protein/min
|
[44]
|
|
MATE2‐K
|
K m = 8.2 ± 1.8 μM V max = 297.3 ± 6.2 pmol/mg protein/min
|
[44]
|
3.3.2.2 Platinum Drugs
Platinum‐based anticancer drugs are also substrates of MATE transporters with preference of cisplatin for hMATE1 and rMate1 and oxaliplatin for hMATE2‐K [37, 38]. Treatment of Mate1 knockout mice with cisplatin increased renal platinum accumulation and heightened susceptibility to cisplatin‐induced nephrotoxicity compared with wild‐type mice [39]. Similar results were reported in mice treated with a pharmacological inhibitor of Mate1 [39]. In addition to causing renal damage, platinum‐based drugs are also well known for the ability to cause peripheral neuropathy. Treatment of rats with oxaliplatin and rMate1 siRNA injections increased platinum accumulation in the dorsal root ganglion, as well as the extent of peripheral neuropathy compared with that of rats receiving only oxaliplatin [40]. Taken together, these data point to the ability of Mate transporters to regulate the toxicities associated with platinum drugs.
3.3.2.3 Cardiovascular Drugs
A number of drugs that alter cardiovascular function are substrates for MATE transporters. For example, beta‐adrenergic
