11-deoxy-15-keto-13,14-dihydro-11 beta,16-cycloprostaglandin E2

degradation product of 15-keto-13,14-dihydro-PGE2; structure in first source

Also Known As:

11-deoxy-13,14-dihydro-15-keto-11 beta,16 xi-cyclo-PGE2; 11-deoxy-15-keto-13,14-dihydro-11 beta, 16-cyclo-PGE2; DKDBCYPGE2; PGE2-M; PGEM-II; bicyclo-PGEM; 5-Heptenoic acid, 7-(4-butyloctahydro-2,5-dioxo-1H-inden-1-yl)-

Networked: 7 relevant articles (0 outcomes, 0 trials/studies)

Bio-Agent Context: Research Results

Related Diseases

1.	Neoplasms (Cancer) 12/01/1984 - "The increases in plasma calcium and PGE2-M observed in tumor-bearing mice were the same on both normal and very low calcium intakes. " 08/01/1977 - "Both the rate of rise and magnitude of the increase were greater for the metabolite than for PGE2; at the time of peak hyercalcemia (about 4 to 5 weeks after tumor implantation), the increase over basal in plasma PGE2-M was about 75 fold whereas it was previously shown that the increase in PGE2 was less than 2 fold. " 04/01/1978 - "2 wk after tumor implantation, plasma PGE2-M and ceruloplasmin had risen about 20- and 6-fold, respectively, while the rise in plasma calcium was just beginning. " 08/01/1977 - "Indomethacin, which inhibits PGE2 synthesis in VX2 cells in culture, lowered in parallel plasma calcaium and PGE2-M in tumor-bearing rabbits. " 08/01/1977 - "Administration of hydrocortisone to rabbits bearing the VX2 tumor prevented the development of hypercalcemia when given at the time of tumor implantation and reversed the elevated plasma calcium in previously untreated animals; the steroid hormone also lowered plasma concentrations of PGE2-M. "
2.	Hypercalcemia (Milk Alkali Syndrome) 04/01/1978 - "Plasma ceruloplasmin and PGE2-M rose in parallel (within 7-10 days) and preceded by 7-10 days the development of hypercalcemia. " 08/01/1977 - "Administration of hydrocortisone to rabbits bearing the VX2 tumor prevented the development of hypercalcemia when given at the time of tumor implantation and reversed the elevated plasma calcium in previously untreated animals; the steroid hormone also lowered plasma concentrations of PGE2-M. "
3.	Pelvic Pain 11/01/1986 - "The lack of change in bicyclo PGEM and PGFM in peripheral plasma would suggest a local transfer of PGs produced by injured tubal tissue to other parts of the tube and the uterus resulting in increased contractions and pelvic pain."
4.	Hypotension (Low Blood Pressure) 08/01/1990 - "Hypotension was also evident in a subgroup of pregnant rabbits (n = 4) with low PGE2-M concentrations in the nonpregnant range (3.2 +/- 1.5 ng/ml vs 1.9 +/- 1.2 in nonpregnant rabbits, ns). " 08/01/1990 - "On the 23rd dg hypotension was invariably present (61 +/- 5 mmHg vs 72 +/- 4 in nonpregnants, p less than 0.001), but arterial levels of PGE2-M (31.0 +/- 31.6 ng/ml) did not overcome those measured on earlier, normotensive days of gestation. " 08/01/1990 - "Since the arterial level of PGE2-M proved to correlate (p less than 0.001) with both the uteroplacental venous and renal venous PGE2 concentrations, we suggest that a key role of uteroplacental and renal PGE2 played in the development of gestational hypotension is not probable in rabbits."
5.	Essential Hypertension 01/01/1986 - "Acute and chronic effects of captopril on bicyclo-PGEm, the stable bicyclic end product of prostaglandin E2 in essential hypertension."

Related Drugs and Biologics

1.	Dinoprostone (PGE2)
2.	Calcium
3.	Steroids
4.	Prostaglandins
5.	Indomethacin (Indometacin)
6.	Hydrocortisone (Cortisol)
7.	Hormones (Hormone)
8.	Ceruloplasmin (Ferroxidase)
9.	Captopril (Capoten)
10.	15-keto-13,14-dihydroprostaglandin F2alpha (PGFM)