The present invention relates generally to variants and peptides of the mitochondrial protein, voltage-dependent anion channel (VDAC) and to polynucleotides encoding same. In particular, the present invention is directed to N-terminal truncated and mutated VDAC and specific amino acid and polynucleotide sequences thereof useful in inhibiting apoptosis, and to pharmaceutical compositions comprising same useful in the treatment of diseases associated with excess apoptosis.