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Richard D. May

Researcher at Southern Research Institute

Publications -  11
Citations -  558

Richard D. May is an academic researcher from Southern Research Institute. The author has contributed to research in topics: Saponin & Quillaja saponaria. The author has an hindex of 7, co-authored 11 publications receiving 539 citations.

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Development of semisynthetic triterpenoid saponin derivatives with immune stimulating activity.

TL;DR: New semi-synthetic analogs were developed that have the adjuvanticity of quillaja saponins, yet with less toxicity and greater stability in aqueous solutions, as well as CTL production against exogenous antigens.
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Differential toxicity of camptothecin, topotecan and 9-aminocamptothecin to human, canine, and murine myeloid progenitors (CFU-GM) in vitro

TL;DR: The greater susceptibility of humans and dogs to the myelotoxicity of camptothecins, compared to mice, was evident in vitro at the cellular level, explaining why the curative doses of TPT and 9AC in mice with human tumor xenografts are not achievable in patients.
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Altered immunomodulating and toxicological properties of degraded Quillaja saponaria Molina saponins.

TL;DR: Modification of the immune-modulating properties brought by the degradation of quillaja saponins during vaccine storage may change the intended immune response from a Th1 to a Th2 type, which would have negligible effects on vaccines depending on Th2 immunity mediated by neutralizing antibodies.
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Fractionation, structural studies, and immunological characterization of the semi-synthetic Quillaja saponins derivative GPI-0100.

TL;DR: The strong immune stimulatory properties of RP 18-2, relative to RP18-1, and the formation of RP18/RP18-2 mixed micelles may account for the effective stimulation of Th1 immunity by UFGPI-0100.
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Reduced proliferation of non-megakaryocytic acute myelogenous leukemia and other leukemia and lymphoma cell lines in response to eltrombopag.

TL;DR: It is suggested that eltrombopag does not enhance, but rather inhibits, proliferation of leukemia cell lines in vitro, and appears to be through a TpoR-independent, nonapoptotic mechanism.