Not sure why period are afraid of sourcing from China. Lots of great peptides and AAS coming from there. You just have to know the good sources.
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This is a bit out of my wheelhouse, but here’s a few:
List of Vendors:
- Shanghai Pemichem Biotechnology Co., Ltd.: Supplies 99% pure 17α-estradiol raw powder; based in Shanghai.
- Shandong Octagon Chemicals Limited (Octagonchem): One of the largest manufacturers in China; offers kilos in stock for prompt shipment.
- Zhengzhou Key-chemi Bioscience Co., Ltd.: Trader supplying 17α-estradiol; located in Zhengzhou.
- Shanghai Jizhi Biochemical Technology Co., Ltd.: Offers 98% purity product at around ¥568/200mg; Shanghai-based.
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Thanks. I guess the way to begin is to start compiling places that hold it, the link to their page and price information.
I’d also say finding out who is willing to offer a sample is good.
If we can get some good information compiled then it might be worth figuring out logistics.
I’ve emailed about 8 places. As of now I’ve got:
Shandong Octagon Chemicals Limited
Price: 1200 USD for 100 G including the shipping cost
I imagine there will be cheaper options.
I’ve also contacted Janoshik and asked if they’re able to test 17 alpha estradiol and find out purity and if there is 17 beta estradiol contamination.
There’s actually a REALLY long list when I put it through the various ‘searching’ LLMs. I just wish I knew which suppliers already have a good reputation.
Don’t trust LLMs for this. It needs to be done manually.
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I think it’s worth pointing out that a number of papers incorrectly claim that 17α-E2 and 17β-E2 are enantiomers, which would imply that they have identical physical properties.
Enantiomers are inverted at all chiral centers, whereas 17α-E2 and 17β-E2 are only inverted at C17, which makes them diastereomers. Because of this they have different physical properties, which in principle usually makes them easier to separate, although in practice it can still be quite difficult.
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I’m reaching out to see how many people are actually interested in participating in this group buy if we end up doing it?
I’m interested. Who else?
I’m still hearing back from different vendors.
I’ve heard back from Janoshik on testing, but maybe people know other vendors that might be more appropriate for this task.
My thoughts are we get samples from all vendors that seem good, send those to a testing facility. The one that comes up best we then do a group buy. We figure out how much of the molecule everyone wants and make the order.
I’ve never done a group buy though, so I’m not 100% sure on the logistics of this from that point onwards so hopefully someone more experienced can help explain this process.
Are you in Australia? That would complicate things greatly. Australian customs is notorious.
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Yes I agree. If enough people are interested we may be able to have someone else actually ship things out. I would rather not run it all through Australia any more than necessary.
Premenopausal women are less sensitive than men or postmenopausal women to acute kidney injury (AKI), which is characterized by renal tubule ferroptosis and nephron loss. Tonnus et al . uncovered two mechanisms through which estrogen limited ferroptosis of renal tubule cells in female mice after ischemia-reperfusion injury (IRI). Renal IRI induced more tubule ferroptosis in male and ovariectomized females compared with intact females, and treatment with a pharmacological inhibitor of ferroptosis reduced kidney damage in male, but not female, mice. Two hydroxylated derivatives of 17β-estradiol, 2OH-E2 and 4OH-E2, protected cultured cells from pharmacological induction of ferroptosis, acted as radical-trapping antioxidants in vitro, and were enriched in the renal tubules of female mice. In renal tubules explanted from mice after IRI, 2OH-E2 protected male tissues against cell damage and death but did not further protect female tissues. Genomic actions of estrogen also contributed to its protective effects, because female mice lacking the intracellular 17β-estradiol receptor ESR1 showed more tubule ferroptosis and kidney damage in response to renal IRI compared with wild-type female mice. ESR1-mediated genomic estrogen signaling reduced both the turnover of the endogenous antiferroptotic molecule GSSH and the biosynthesis of ether lipids, which are substrates for peroxidation and increase the susceptibility to ferroptosis. Experiments in male and ovariectomized female mice and in renal biopsies from male, premenopausal female, and postmenopausal female patients were consistent with these protective genomic effects of estrogen being absent in male and postmenopausal females. Thus, estrogen protects against ferroptosis and AKI through both nongenomic and genomic mechanisms.