الفهرس 
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Abstract
The investigable marine organisms in this study were collected from different places. Stylissa carteri was collected from the Red Sea (Hurghada, Egypt), Dysldea avara was collected from the Mediterranean Sea (Turkey), as well as Acanthostylotella sp. was collected from the Indian Ocean (Bali, Indonesia).
8.1. Summary of the work.
The work is divided into two main parts: 8.1.1. Summary of the isolated compounds:
27 compounds were isolated from the marine sponges; Stylissa carteri, Dysidea avara as well as Acanthostylotella sp. All are known except (_) N-methylmelemelone A (Dysidea avara sponge).
The isolated compounds are summarized in the following (Tab., 62-64):
8.1.2. Biological activities of the isolated compounds:
The isolated compounds were submitted to three different biological activities. They were summarized as follow:
8.1.2.1. Cytotoxicity test:
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8.1.2.1. 1. Mouse lymphoma cell line L5178Y:
Most of the isolated compounds were submitted to cytotoxicity using mouse lymphoma cell line (L5178Y). The results are summarized as follow:
(+)-Avarol and avarone derivatives except (-) N-methylmelemelone A
~
and (-)-4’ -methylaminoavarone proved to be highly active against
L5178Y cell line. On the other hand, Z-3-bromohymenialdisine, (+) dibromophakellin, (- )-4’ -methylaminoavarone and 3,4-dibromo-lH pyrrole-2-methylcarboxylate showed moderate cytotoxic activity. 3,4-
,
dibromo-lH-pyrrole-2-carbamide, Z-hymenialdisine, Z-spongiacidin D,
(- )-clathramide C, (-)- N-methylmelemelone A, (+ )-longamide and mukanadin D exhibited weak cytotoxic activity.
.1.2.2. Protein kinase inhibition:
Many of the isolated compounds were tested on 24 different types of protein kinases and measeure the residual activity. The results are summarized as follow:
(+)-Manzacidin A showed weak inhibition to protein kinase; AKTl. Agelongine exhibited ~eak inhibition to protein kinase; AKTI and moderate to FLT3. 3,4-Dibromo-lH-pyrrole-2-carbamide showed weak inhibition to protein kinases; 4Aurora-B, 12EGF-R, 15FAK, 16IGFI-R, 23SRC and 24VEGF-R2. E-Debromohymenialdisine showed weak inhibition to protein kinases; 2ARK5, 7CDK2/CycA, 8CDK4/CycDl, 19PDGFR-beta, 20PLKl, 22SAK and 24VEGF-R2. Z-Hymenialdisine showed weak inhibition to protein kinases; 7CDK2/CycA,