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4-Amino-3-hydroxybenzoic acid


  • Brand : BIOFRON

  • Catalogue Number : BN-O1160

  • Specification : 98%(HPLC)

  • CAS number : 2374-03-0

  • Formula : C7H7NO3

  • Molecular Weight : 153.14

  • PUBCHEM ID : 137566

  • Volume : 5mg

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Catalogue Number


Analysis Method





Molecular Weight



Botanical Source

Structure Type





4-Amino-3-hydroxy benzoic acid/2-hydroxyaniline/Benzoic acid, 4-amino-3-hydroxy-/2-Amino-5-carboxyphenol/4-Amino-3-hydroxybenzoic acid/3-hydroxy-4-aminobenzoate/2hdr/2-hydroxy-4-carboxyaniline/3-hydroxy-4-amino-benzoic acid


4-amino-3-hydroxybenzoic acid


1.5±0.1 g/cm3


Flash Point

187.1±26.5 °C

Boiling Point

385.7±37.0 °C at 760 mmHg

Melting Point

211-215 °C(lit.)


InChl Key


WGK Germany


HS Code Reference

Personal Projective Equipment

Correct Usage

For Reference Standard and R&D, Not for Human Use Directly.

Meta Tag

provides coniferyl ferulate(CAS#:2374-03-0) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

No Technical Documents Available For This Product.




Acute kidney injury (AKI) can lead to chronic kidney disease (CKD) if injury is severe and/or repair is incomplete. However, the pathogenesis of CKD following renal ischemic injury is not fully understood. Capillary rarefaction and tubular hypoxia are common findings during the AKI-to-CKD transition. We investigated the tubular stress response to hypoxia and demonstrated that a stress-responsive transcription factor, FoxO3, was regulated by prolyl hydroxylase (PHD). Hypoxia inhibited FoxO3 prolyl hydroxylation and FoxO3 degradation, leading to FoxO3 accumulation and activation in tubular cells. Hypoxia-activated HIF-1α contributed to FoxO3 activation and functioned to protect kidneys, as tubular deletion of HIF-1α decreased hypoxia-induced FoxO3 activation and resulted in more severe tubular injury and interstitial fibrosis following ischemic injury. Strikingly, tubular deletion of FoxO3 during the AKI-to-CKD transition aggravated renal structural and functional damage, leading to a much more profound CKD phenotype. We show that tubular deletion of FoxO3 resulted in decreased autophagic response and increased oxidative injury, which may explain renal protection by FoxO3. Our study indicates that in the hypoxic kidney, stress-responsive transcription factors can be activated for adaptions to counteract hypoxic insults, thus attenuating CKD development.


Keywords: Cell Biology, Nephrology Keywords: Autophagy, hypoxia


FoxO3 activation in hypoxic tubules prevents chronic kidney disease


Ling Li,1 Huimin Kang,1,2 Qing Zhang,3 Vivette D. D’Agati,4 Qais Al-Awqati,5 and Fangming Lincorresponding author1

Publish date

2019 Jun 3;




When a human being is placed for several days on a completely defined diet, consisting almost entirely of small molecules that are absorbed from the stomach into the blood, intestinal flora disappear because of lack of nutrition. By this technique, the composition of body fluids can be made constant (standard deviation about 10%) after a few days, permitting significant quantitative analyses to be performed. A method of temperature-programmed gas-liquid partition chromatography has been developed for this purpose. It permits the quantitative determination of about 250 substances in a sample of breath, and of about 280 substances in a sample of urine vapor. The technique should be useful in the application of the principles of orthomolecular medicine.


Quantitative Analysis of Urine Vapor and Breath by Gas-Liquid Partition Chromatography


Linus Pauling,* Arthur B. Robinson,* Roy Teranishi,† and Paul Cary*

Publish date

1971 Oct;




Inbred Lewis (LEW/N) female rats develop an arthritis in response to group A streptococcal cell wall peptidoglycan polysaccharide (SCW), which mimics human rheumatoid arthritis. Histocompatible Fischer (F344/N) rats do not develop arthritis in response to the same SCW stimulus. To evaluate this difference in inflammatory reactivity, we examined the function of the hypothalamic-pituitary-adrenal (HPA) axis and its ability to modulate the development of the inflammatory response in LEW/N and F344/N rats. We have found that, in contrast to F344/N rats, LEW/N rats had markedly impaired plasma corticotropin and corticosterone responses to SCW, recombinant human interleukin 1 alpha, the serotonin agonist quipazine, and synthetic rat/human corticotropin-releasing hormone. LEW/N rats also had smaller adrenal glands and larger thymuses. Replacement doses of dexamethasone decreased the severity of LEW/N rats’ SCW-induced arthritis. Conversely, treatment of F344/N rats with the glucocorticoid receptor antagonist RU 486 or the serotonin antagonist LY53857 was associated with development of severe inflammatory disease, including arthritis, in response to SCW. These findings support the concept that susceptibility of LEW/N rats to SCW arthritis is related to defective HPA axis responsiveness to inflammatory and other stress mediators and that resistance of F344/N rats to SCW arthritis is regulated by an intact HPA axis-immune system feedback loop.


Inflammatory mediator-induced hypothalamic-pituitary-adrenal axis activation is defective in streptococcal cell wall arthritis-susceptible Lewis rats.


E M Sternberg, J M Hill, G P Chrousos, T Kamilaris, S J Listwak, P W Gold, and R L Wilder

Publish date

1989 Apr;

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