Table 1 Biological evaluation of bryostatin analogs.

From: Synthesis and evaluation of designed PKC modulators for enhanced cancer immunotherapy

Compound

Ki PKCα (nM)

Ki PKCδ (nM)

% Translocation (concentrationa)

Fold increase CD22 expressionb

Bryostatin 1

0.8

1.1

70% (200 nM)

2.10

SUW200

4.1

7.6

70% (200 nM)

1.73

SUW201

0.54

1.4

65% (200 nM)

1.59

SUW203

1.0

4.1

50% (1000 nM)

1.16

SUW204

1.4

3.7

25% (200 nM)

0.98

SUW206

1.0

1.3

60% (200 nM)

1.63

SUW207

2.0

5.4

60% (200 nM)

1.33

SUW208

1.0

4.7

75% (200 nM)

1.68

SUW209

1.6

3.5

60% (1000 nM)

1.45

SUW210

5.6

7.3

75% (1000 nM)

1.49

SUW211

98

27

20% (1000 nM)

ND

SUW212

40

24

50% (1000 nM)c

ND

SUW217

9.2

9.4

75% (200 nM)

1.97

SUW218

7.1

6.6

55% (200 nM)

1.92

SUW219

37

25

60% (1000 nM)

ND

SUW220

16

15

50% (1000 nM)

ND

SUW226

5.8

6.6

75% (200 nM)

1.76

SUW229

1.8

1.2

50% (200 nM)

2.35

SUW230

4.2

9.4

65% (200 nM)

1.62

  1. Compounds were evaluated for PKC-binding affinity in a competitive binding assay with [3H]-phorbol dibutyrate in PKCα and PKCδ, members of the conventional and novel PKC isoform families, respectively. Cell entry and PKC activation in living cells was determined by monitoring translocation of a PKCδ-GFP fusion protein from the cytosol to the plasma membrane. Representative images included in Fig. 5.
  2. ND not determined.
  3. aIndicates minimum effective concentration required to induce translocation of PKC-GFP to the membrane.
  4. bIn NALM6 cells at 1 nM relative to DMSO control (n = 3 biological replicates).
  5. cIndicates only brief translocation observed (Fig. 5d).
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