It'll be interesting since it's such a low dose relative to the 20mg+ people usually opt for. The major points for emphasis, though, are that injectable Sdrol bypasses first metabolism, yes, but the hepatic strain is a consequence of its 17alpha-methylation. The orally active AAS, with this modification, even injected, have a considerable half-life (hours) and relatively low volume of distribution... Basically, think of first pass as almost irrelevant.
Another question arises from the Vida data on D-45 (Superdrol). Zaffaroni's research on Sdrol indicated that the marked reduction in androgenicity and increase in anabolism from 2alpha-methylation was likely maintained only via the oral route. There is some data from Vida, without specification of route of administration, that this may hold true as well as more recent research stating that the 2alpha-methylation doesn't seem to "hold up" in its potent dissociation between anabolism and androgenicity with injectable androgens.
Here's the table from Vida (it's been suggested that the unspecified route of administration was the oral route, language barrier remaining):
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