"HE 3286" ? A Pre-Clinical DHEA Metabolite
Posted: Sat Dec 02, 2006 6:31 pm
Here’s a link to info about a potential new “pre-clinical” drug for MS, “HE 3286”.
The headline is about Rheumatoid Arthritis but if you read the news release it sounds like it’s been tested in female EAE mice.
My wild speculation, and it is just that, wild speculation, is that “HE 3286” might be a metabolite of DHEA and/or a synthetic form of DHEA.
Per their release, the company “is developing a proprietary new class of small molecules that are metabolites or synthetic analogs of adrenal steroid hormones.” DHEA is synthesized in the adrenal glands. What they say their compounds do (per the investor’s fact sheet quotes below) is consistent with many things I’ve read about DHEA.
This from the company’s investor fact sheet:
Take care all
Sharon
The headline is about Rheumatoid Arthritis but if you read the news release it sounds like it’s been tested in female EAE mice.
My wild speculation, and it is just that, wild speculation, is that “HE 3286” might be a metabolite of DHEA and/or a synthetic form of DHEA.
Per their release, the company “is developing a proprietary new class of small molecules that are metabolites or synthetic analogs of adrenal steroid hormones.” DHEA is synthesized in the adrenal glands. What they say their compounds do (per the investor’s fact sheet quotes below) is consistent with many things I’ve read about DHEA.
This from the company’s investor fact sheet:
If “HE 3286” is a DHEA metabolite, here’s some more info on DHEA I don’t think I’ve posted yet. Some quick takes: Treatment with DHEA Promotes Recovery of Motor Behavior After Spinal Cord InjuryHollis-Eden Pharmaceuticals is developing a proprietary new class of small molecule compounds based on its Hormonal Signaling Technology Platform. These compounds, metabolic conversions or synthetic analogs of adrenal steroid hormones, are designed to restore the biological activity of cellular signaling pathways disrupted by disease and aging. Hollis-Eden has demonstrated in humans that these compounds possess several biological properties with potential therapeutic benefit –they regulate innate and adaptive immunity, reduce nonproductive inflammation, and stimulate cell proliferation and tissue regeneration.
Hollis-Eden's compounds have been shown in preclinical and clinical studies to regulate immune activity against a broad spectrum of disease and pathogens, including viruses, bacteria and parasites.
DHEA Stimulates Neurogenesis in the HippocampusMore strikingly, DHEA enhanced recovery of left-right coordination and fine motor control.
DHEA significantly increased the area of white matter spared at the epicenter and reduced the area of reactive gliosis surrounding the lesion. These data demonstrate the effectiveness of DHEA in promoting functional recovery in the adult murine injured spinal cord.
DHEA and Human Neural Stem CellsThese results show that DHEA, a steroid prominent in the blood and cerebral environment of humans, but which decreases markedly with age and during major depressive disorder, regulates neurogenesis in the hippocampus and modulates the inhibitory effect of increased corticoids on both the formation of new neurons and their survival.
Preclinical Development of Neurosteroids as Neuroprotective Agents for the Treatment of Neurodegenerative DiseasesTogether these data suggest that DHEA is involved in the maintenance and division of human neural stem cells.
I’m going to be watching “HE 3286”. If it is a DHEA metabolite I think it has a lot of potential to help manage MS.DHEAS protects certain neuronal populations against neurotoxic insults inflicted by the excitatory amino acid glutamate (Kimonides et al., 1998; Mao and Barger, 1998). This finding suggests that DHEAS may be useful in treating neurodegenerative diseases in which excitotoxicity is believed to be the underlying cause or a major contributor to cell death. Moreover, because DHEA and DHEAS are multifunctional and exhibit a variety of properties in the CNS, including memory consolidation, neuroprotection, and reduction of neurodegeneration (Majewska, 1992, 1995; Lapchak et al., 2000), their potential therapeutic benefits may be extended to include the treatment of other neurodegenerative diseases not directly linked to excitotoxicity.
Take care all
Sharon