{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
Restrict the search for
angiotensin ii
to a specific field?
Status:
Other
Class (Stereo):
CHEMICAL (RACEMIC)
Targets:
Conditions:
(±)-2,3A-di-epi-Perindopril is a mixture of two isomers (S, SR, RR) and (R, RS, SS) which are both inactive epimers of the antihypertensive drug perindopril, although the (R, RS, SS) isomer possesses better activity.
Status:
Other
Class (Stereo):
CHEMICAL (ACHIRAL)
4-{2-[5-methyl-1-(naphthalen-2-yl)-1H-pyrazol-3-yloxy]ethyl}morpholine (S1RA, E-52862) is an 1-arylpyrazole class of sigma-1 receptor antagonist. Formalin-induced nociception (both phases), capsaicin-induced mechanical hypersensitivity and sciatic nerve injury-induced mechanical and thermal hypersensitivity were dose-dependently inhibited by systemic administration of S1RA. Occupancy of sigma-1 receptors in the CNS was significantly correlated with the antinociceptive effects. As a mechanistic correlate, electrophysiological recordings demonstrated that pharmacological antagonism of sigma-1 receptors attenuated the wind-up responses in spinal cords sensitized by repetitive nociceptive stimulation. Esteve is developing E 52862 for the treatment of several pain indications, including diabetic neuropathies, chemotherapy-induced neuropathic pain, postherpetic neuralgia, postoperative pain. Phase II development of this first-in-class agent is underway in Romania, Spain and Greece.
Status:
Other
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
Grepafloxacin, (R)- is an asymmetric fluoroquinolone derivative which possesses high tissue penetrability as well as strong, broad-spectrum antimicrobial activities. Grepafloxacin has a chiral center and therefore has two optical enantiomeric isomers, R(+)- and S(-)-grepafloxacin. In neutrophil respiratory burst induced by N-formyl-methionyl leucyl-phenylalanine grepafloxacin induces a priming effect. The R(+) enantiomer of grepafloxacin induced a more potent priming effect than did S(-)-grepafloxacin. R(+)-Grepafloxacin also produced a more potent translocation of both p47- and p67-phox proteins to membrane fractions of neutrophils. Grepafloxacin-induced primed superoxide generation was significantly inhibited by pretreatment with PD169316 and SB203580, p38 mitogen-activated protein kinase (MAPK) inhibitors, but not with PD98059, a specific inhibitor of the upstream kinase that activates p44/42 MAPK, or SP600125, an inhibitor of stress-activated protein kinase/c-Jun N-terminal kinase (JNK).
