Overview of CAS 123-30-8

Client Email Product
  • Chemistry
Also known as: P-aminophenol, 123-30-8, 4-hydroxyaniline, P-hydroxyaniline, Phenol, 4-amino-, Paranol
Molecular Formula
Molecular Weight
109.13  g/mol
InChI Key

1 2D Structure


2 Identification
2.1 Computed Descriptors
2.1.1 IUPAC Name
2.1.2 InChI
2.1.3 InChI Key
2.1.4 Canonical SMILES
2.2 Other Identifiers
2.2.1 UNII
2.3 Synonyms
2.3.1 MeSH Synonyms

1. 4-aminophenol Conjugate Monoacid

2. 4-aminophenol Hydrochloride

3. 4-aminophenol Monopotassium Salt

4. 4-aminophenol Monosodium Salt

5. 4-aminophenol Sulfate

6. 4-aminophenol Sulfate (2:1)

7. 4-aminophenol, 18o-labeled

8. 4-aminophenol, 3h-labeled

9. 4-aminophenol, Ion(1+)

10. 4-hydroxyaniline

11. P-aminophenol

12. P-aminophenol Phosphate

13. Para-aminophenol

2.3.2 Depositor-Supplied Synonyms

1. P-aminophenol

2. 123-30-8

3. 4-hydroxyaniline

4. P-hydroxyaniline

5. Phenol, 4-amino-

6. Paranol

7. Certinal

8. Citol

9. Azol

10. 4-aminobenzenol

11. Fouramine P

12. Ursol P Base

13. Rodinal

14. P-hydroxyphenylamine

15. Benzofur P

16. Fourrine P Base

17. Pelagol P Base

18. Tertral P Base

19. Ursol P

20. 4-amino-1-hydroxybenzene

21. Durafur Brown Rb

22. Furro P Base

23. Nako Brown R

24. Renal Ac

25. Fourrine 84

26. Phenol, P-amino-

27. Zoba Brown P Base

28. 4-amino-phenol

29. Unal

30. 1-amino-4-hydroxybenzene

31. Basf Ursol P Base

32. C.i. Oxidation Base 6

33. Pelagol Grey P Base

34. P-aminofenol

35. Para-aminophenol

36. P-aminofenol [czech]

37. Aminophenol, P-

38. Paramidophenol

39. P-aminobenzenol

40. Unii-r7p8frp05v

41. Nsc 1545

42. C.i. 76550

43. Ccris 4146

44. Chebi:17602

45. Hsdb 2640

46. Einecs 204-616-2

47. Mfcd00007869

48. R7p8frp05v

49. Ci 76550

50. Ai3-14872

51. C.i. Oxidation Base 6a

52. Plikawjenqzmha-uhfffaoysa-n

53. P-aminophenol [un2512] [poison]

54. Ncgc00090816-01

55. Ncgc00090816-02

56. 4-aminophenol, 97%

57. Dsstox_cid_4499

58. Dsstox_rid_77429

59. Dsstox_gsid_24499

60. 4nl

61. Cas-123-30-8

62. Paraaminophenol

63. Energol

64. Kodelon

65. Takatol

66. Para Aminophenol

67. Aj-333/25022099

68. P-amino-phenol

69. 4-amino Phenol

70. 4-aminophenol B

71. 4-aminophenol?

72. Para-amino-phenol

73. 4-hydroxy-aniline

74. Para-hydroxyaniline

75. Para Amino Phenol

76. 4-hydroxyphenylamine

77. Phenol Derivative, 9

78. Furro P (salt/mix)

79. Pubchem22199

80. Peltol P (salt/mix)

81. Acmc-209aoj

82. Pelagol Cp (salt/mix)

83. Futramine P (salt/mix)

84. Wln: Zr Dq

85. Bmse000462

86. Epitope Id:117708

87. Ec 204-616-2

88. 4-aminophenol, >=98%

89. Schembl3424

90. Chembl1142

91. Durafur Brown R (salt/mix)

92. Ksc354q5h

93. Mls001066356

94. Pelagol Grey Cp (salt/mix)

95. Ac1l195p

96. Ac1q523t

97. Ac1q523u

98. Sgcut00256

99. Dtxsid3024499

100. Schembl15663694

101. Bdbm26195

102. Nsc1545

103. Bcp25857

104. Ks-000000hn

105. Nsc-1545

106. To_000006

107. Zinc4623758

108. 4-aminophenol, >=99% (hplc)

109. Tox21_113242

110. Tox21_113477

111. Tox21_201030

112. Anw-18113

113. Bbl011574

114. Ls-676

115. P-aminophenol [un2512] [poison]

116. Sbb059792

117. Stk286017

118. 4-aminophenol, Technical Grade, 95%

119. Akos000119829

120. Akos016371265

121. Tox21_113477_1

122. Am86423

123. As04549

124. Mcule-3319647085

125. Rp18925

126. Tra0083709

127. Un 2512

128. Ncgc00090816-03

129. Ncgc00090816-04

130. Ncgc00090816-05

131. Ncgc00258583-01

132. Aj-51764

133. An-22912

134. An-24398

135. As-54109

136. Bc227837

137. Cj-12175

138. I924

139. Sc-19013

140. Smr000471841

141. St088538

142. Ab1009438

143. St2405553

144. Tr-003672

145. A0384

146. Cs-0006652

147. Ft-0617593

148. 9225-ep2275420a1

149. 9225-ep2280008a2

150. 9225-ep2308872a1

151. 9225-ep2316829a1

152. C02372

153. L-1224

154. 135807-ep2371803a1

155. 135807-ep2377843a1

156. 4-aminophenol, Pestanal(r), Analytical Standard

157. I01-0483

158. J-004908

159. J-514454

160. Z57127517

161. F2190-0438

162. Unii-lst7140d72 Component Plikawjenqzmha-uhfffaoysa-n

163. 4-aminophenol, United States Pharmacopeia (usp) Reference Standard

164. Inchi=1/c6h7no/c7-5-1-3-6(8)4-2-5/h1-4,8h,7h

165. Mesalazine Impurity A, European Pharmacopoeia (ep) Reference Standard

166. 4-aminophenol, 250 Mug/ml In Acetonitrile, Certified Reference Material, Ampule Of 1 Ml

167. 1-amino-4-hydroxybenzene 4-amino-1-hydroxybnzene 4-aminobenzenol 4-amino-pheno

168. 4-aminophenol (acetaminophen Related Compound K) (paracetamol Impurity K), Pharmaceutical Secondary Standard; Certified Reference Material

2.4 Create Date
3 Chemical and Physical Properties
Molecular Weight 109.13 g/mol
Molecular Formula C6H7NO
Hydrogen Bond Donor Count2
Hydrogen Bond Acceptor Count2
Rotatable Bond Count0
Exact Mass109.052764 g/mol
Monoisotopic Mass109.052764 g/mol
Topological Polar Surface Area46.2 A^2
Heavy Atom Count8
Formal Charge0
Isotope Atom Count0
Defined Atom Stereocenter Count0
Undefined Atom Stereocenter Count0
Defined Bond Stereocenter Count0
Undefined Bond Stereocenter Count0
Covalently Bonded Unit Count1
4 Drug and Medication Information
4.1 Minimum/Potential Fatal Human Dose

4.4 = very toxic: probable oral lethal dose (human) 50-500 mg/kg, between 1 teaspoon & 1 oz for 70 kg person (150 lb). ... causes methemoglobinemia, but less toxic than aniline in animals. ... diln used in photography do not have significant percutaneous toxicity in most cases.

Gosselin, R.E., H.C. Hodge, R.P. Smith, and M.N. Gleason. Clinical Toxicology of Commercial Products. 4th ed. Baltimore: Williams and Wilkins, 1976., p. II-141

5 Pharmacology and Biochemistry
5.1 MeSH Pharmacological Classification


Chemical agents that increase the rate of genetic mutation by interfering with the function of nucleic acids. A clastogen is a specific mutagen that causes breaks in chromosomes. (See all compounds classified as Mutagens.)

5.2 Absorption, Distribution and Excretion

An absorption and excretion study of permanent hair dye intermediates containing 14-C was conducted in hairless Wistar rats under conditions of oxidation hair dyeing (ie, intermediates were mixed with H202 immediately before application). The cutaneous penetration of 14C-4-aminophenol (PAP) alone and in admixture with a nonradioactive coupler (3-amino-6-methylphenol, a 3-aminophenol (MAP) derivative) and that of the resultant 14C-indamine (N-[4-hydroxyphenyl}-3-amino-6-methyl benzoquinone imine) was determined. Hair dye solutions containing uniformly labeled PAP (0.75% or 70 nM) in a simple vehicle were applied to a 10 sq cm dorsal surface of up to 5 rats. Doses of PAP of 0.14 uM/sq cm, 0.69 uM/sq cm, and 3.44/ uM/sq cm yielded respective concentrations of 15.9 +/- 4.76 nM/sq cm, 52.04 +/- 6.73 nM/sq cm, and 58.4 +/- 11.5 nM/sq cm, which penetrated the skin and were detected in the excreta, the viscera, and the skin (excluding PAP found at the site of application) of the treated rats after 4 days. At the highest 14C-PAP concentration applied, the total quantity of 14C-PAP detected per sq cm of skin was approximately the same for PAP alone as for PAP mixed with nonradioactive MAP coupler (56.8 +/- 4.0 nM/sq cm). Penetration of the 14C-indamine was approximately 17 times less (3.6 +/- 0.46 nM) than that of PAP or of the mixture of PAP with the nonradioactive coupler..

Cosmetic Ingredient Expert Review Panel; Final Report on the Safety Assessment of p-Aminophenol, m-Aminophenol, and o-Aminophenol; Journal of the American College of Toxicology 7 (3): 279-333 (1988).

5.3 Metabolism/Metabolites

... Hepatocytes prepared from male Sprague-Dawley rats ... converted para-aminophenol (PAP) to two major metabolites (PAP-GSH conjugates and PAP-N-acetylcysteine conjugates) and several minor metabolites [PAP-O-glucuronide, acetaminophen (APAP), APAP-O-glucuronide, APAP-GSH conjugates, and 4-hydroxyformanilide]. Preincubating hepatoyctes with 1-aminobenzotriazole, an inhibitor of cytochromes P450, did not alter the pattern of PAP metabolism. In conclusion, we found that PAP was metabolized in hepatocytes predominantly to PAP-GSH conjugates and PAP-N-acetylcysteine conjugates in sufficient quantities to account for the nephrotoxicity of PAP. PubMed Abstract

Yan Z et al; Drug Metab Dispos 28 (8): 880-6 (2000)

... The hepatic metabolism of p-aminophenol in Wistar rats and the cytotoxicity of formed glutathione S-conjugates in rat renal epithelial cells /were examined/. After ip application of p-aminophenol (100 mg/kg), the following metabolites were identified in rat bile: 4-amino-2-(glutathion-S-yl)phenol, 4-amino-3-(glutathion-S-yl)-phenol, 4-amino-2,5-bis(glutathion-S-yl)phenol, 4-amino-2,3,5(or 6)-tris(glutathion-S-yl)phenol, an aminophenol conjugate (likely a sulfate or glucuronide), acetaminophen glucuronide, and 3-(glutathion-S-yl)acetaminophen. 4-Amino-3-(glutathion-S-yl)phenol, 4-amino-2,5-bis(glutathion-S-yl)phenol, and 4-amino-2,3,5(or 6)-tris(glutathion-S-yl)phenol induced a dose- and time-dependent loss of cell viability in rat kidney cortical cells. Cell killing was significantly reduced by inhibition of gamma-glutamyl transpeptidase with Acivicin. p-Aminophenol was also toxic to renal epithelial cells. Coincubation of p-aminophenol with tetraethylammonium bromide, a competitive inhibitor of the organic cation transporter, and with SKF-525A, an inhibitor of cytochrome P450, protected cells from p-aminophenol-induced toxicity. p-Aminophenol would thus be accumulated in the kidney mainly by organic cation transport systems, which are concentrated in the S-1 segment of the proximal tubule. However, p-aminophenol toxicity in vivo is directed toward the S-2 and S-3 segments, which are rich in gamma-glutamyl transpeptidase. These results and the observation that biliary cannulation and glutathione depletion reduce p-aminophenol nephrotoxicity suggest that the biosynthesis of toxic glutathione conjugates is responsible for p-aminophenol nephrotoxicity in vivo. The aminophenol glutathione S-conjugates formed induce p-aminophenol nephrotoxicity by a pathway dependent on gamma-glutamyl transpeptidase. PubMed Abstract

Klos C et al; Toxicol Appl Pharmacol 115 (1): 98-106 (1992)

4-Aminophenol in the presence of oxyhemoglobin forms numerous adducts with glutathione (GSH). Using (14)C-4-aminophenol and (3)H-glutathione, ten different thioethers were isolated, by HPLC, with isotope ratios of 1:1, 1:2, 1:3, respectively ... In erythrocytes of humans and dogs, and in dog blood, in vivo, the same pattern of 4-aminophenol conjugates with GSH was found. In vivo, 5% of administered 4-aminophenol is converted into thioethers within erythrocytes, accompanied by a 60% decrease in the cellular GSH, indicating the role of erythrocytes in the biotransformation of xenobiotics. PubMed Abstract

Eckert KG; Xenobiotica 18 (11): 1319-26 (1988)

p-Aminophenol yields p-acetamidophenol, p-aminophenyl-beta-d-glucuronide, p-aminophenyl sulfate, 4-aminoresorcinol, and p-methylaminophenol in rabbit.

European Commission, ESIS; IUCLID Dataset, 4-Aminophenol (123-30-8) p.15 (2000 CD-ROM edition). Available from, as of May 17, 2010:

P-aminophenol yields 4-aminocatechol in rabbit; yields p-quinone in Drosophila. /From table/

Goodwin, B.L. Handbook of Intermediary Metabolism of Aromatic Compounds. New York: Wiley, 1976., p. A-48

4-Aminophenol (PAP) was conjugated at the phenolic group with sulfate or glucuronic acid. PAP may also be N-acetylated to N-acetyl-p-aminophenol (APAP), also known as acetaminophen (Tylenol). Subcutaneous doses of PAP-HCI (0-400 mg/kg) given to Fischer 344 and Sprague-Dawley rats were metabolized to acetylates, sulfates, glucuronides, and other conjugates of both PAP and its metabolite APAP.

Cosmetic Ingredient Expert Review Panel; Final Report on the Safety Assessment of p-Aminophenol, m-Aminophenol, and o-Aminophenol; Journal of the American College of Toxicology 7 (3): 279-333 (1988).

The metabolism of 4-Aminophenol (PAP) was studied in vitro using a clonal strain of rat hepatoma cells (MH1C1). The rate of PAP disappearance was directly related to substrate concentrations, which were between 0.25 mM and 0.75 mM PAP, and incubation times up to 5 hr. The PAP glucuronide appearance rate versus time curve reportedly never reached linearity due to a reaction lag that increased with increasing substrate concentrations, indicating the possible existence of other PAP metabolizing pathways with different substrate optima. The highest rate of PAP-glucuronide formation was at a PAP concentration of 0.5 mM, decreasing at higher concentrations, indicative of possible substrate inhibition of various steps in glucuronidation (eg, uptake, transport, enzymatic coupling). The amount of glucuronide formed per amount of PAP disappearing by the MH1C1 rat hepatoma cells was higher than that formed by R5 clonal rat fibroblast cells (87.7% versus 40%, respectively in umol/mg cell protein/hr). The Chang cell line derived from human liver tissue did not produce any PAP-glucuronide although some of the substrate disappeared.

Cosmetic Ingredient Expert Review Panel; Final Report on the Safety Assessment of p-Aminophenol, m-Aminophenol, and o-Aminophenol; Journal of the American College of Toxicology 7 (3): 279-333 (1988).

The effect of glucuronic acid and glucuronamide administration on the glucuronidation and urinary excretion of 4-aminophenol (PAP) and phenol was studied in rats. Either PAP or phenol at a dose of 300 mg/kg was administered 24 hr after the initial administration of 200 mg/kg glucuronic acid or glucuronamide. Glucuronamide and, to a lesser extent, glucuronic acid increased the excretion of PAP and of PAP-glucuronide in rats receiving PAP. The results after phenol administration were similar.

Cosmetic Ingredient Expert Review Panel; Final Report on the Safety Assessment of p-Aminophenol, m-Aminophenol, and o-Aminophenol; Journal of the American College of Toxicology 7 (3): 279-333 (1988).

p-Aminophenol is considered a minor nephrotoxic metabolite of acetaminophen in humans. Long-term use of acetaminophen can result in an increased lipofuscin deposition in kidneys. In vitro studies have demonstrated that p-aminophenol can undergo oxidative polymerization to form melanin, a component of soluble lipofuscin. Hemolysis accompanies this process in whole blood. Long-term excessive use of phenacetin or acetaminophen has been associated with chronic renal disease, hemolytic anemia, and increased solid lipofuscin deposition in tissues ... .

Clayton, G.D., F.E. Clayton (eds.) Patty's Industrial Hygiene and Toxicology. Volumes 2A, 2B, 2C, 2D, 2E, 2F: Toxicology. 4th ed. New York, NY: John Wiley & Sons Inc., 1993-1994., p. 973

The metabolic capacity of rat brain slices for m-dinitrobenzene (m-DNB) was assessed. ... The m-DNB was metabolized in the brain tissues & the liver tissue. ... Metabolic disposal of m-DNB was 1.05+/-0.11 micromoles/gram (micromol/g) wet weight/hr in the liver, 0.49+/-0.05micromol/g wet weight/hr in brain stem, & 0.44+/0.05micromol/g wet weight/hr in the forebrain. The main metabolite produced by both brain & liver slices was m-nitroaniline, which represented 57 to 66% of the disposal of m-DNB. In the liver, 2-aminophenol, 4-aminophenol, 4-nitrophenol, or 2-nitrophenol was produced, but they were not detected in the brain slices. Nitrosonitrobenzene was detected in slices from both parts of the brain, but not in the liver slices. ... The brain has considerable nitroreductive capacity towards m-DNB & in-situ reduction of m-DNB may be responsible for its neurotoxicity. PubMed Abstract

Hu H-L et al.; Neurotoxicology 18 (2): 363-370 (1997)

The in vitro enzymatic metab of N-nitroso-N-methylaniline (NMA) was investigated using cytochromes P450 2B1 & P450 2B2, isolated from liver microsomes of rats pretreated with phenobarbital (PB), reconstituted with NADPH-cytochrome P450 reductase & dilauroylphosphatidylcholine. Formaldehyde is produced by both cytochromes P450 (P450). NMA is a better substrate for P450 2B1 than for P450 2B2. ... Beside formation of formaldehyde, aniline & p-aminophenol (p-AP) are found to be metabolites formed from NMA by both P450 isoenzymes. ... PubMed Abstract

Stiborova M et al; Cancer Letters 110 (1-2): 11-17 (1996)

The demethylation of N-nitrosodimethylamine (NDMA) & N-nitrosomethylaniline (NMA) is catalyzed by horseradish peroxidase in the presence of hydrogen peroxide. NMA is a better substrate for peroxidase than NDMA. ... The oxidation of NDMA & NMA is inhibited by radical trapping agents (nitrosobenzene, glutathione, ascorbate, NADH). This indicates the radical mechanism for the peroxidase-mediated oxidation of both N-nitrosamines. ... Beside formaldehyde, the metabolites formed from NMA by peroxidase include aniline, p-aminophenol & phenol. Phenol formation presumably arose from N-demethylation of NMA via a benzenediazonium ion (BDI) intermediate while aniline & p-aminophenol from denitrosation of this carcinogen. ... PubMed Abstract

Stiborova M et al; General Physiology and Biophysics 16 (3): 285-297 (1997)

5.4 Mechanism of Action

... Markers of ER stress (XBP1 messenger RNA processing and protein expression; GRP78 and GRP94 upregulation) and ER-mediated cell death (caspase-12 and calpain activation) were examined in kidney tissue of rats exposed to nephrotoxic doses of cisplatin (CIS), gentamicin (GEN), and p-aminophenol (PAP), a nephrotoxic metabolite of acetaminophen. XBP1 signaling was observed with all three drugs and was associated with increased expression of GRP94 and GRP78 in GEN- and PAP-treated animals, but not after CIS exposure. m-Calpain expression was increased after 7 days of CIS treatment, whereas it was decreased in PAP-treated rats. Caspase-12 cleavage products were increased after CIS, GEN, and PAP administration. The results of this study demonstrate that three clinically relevant nephrotoxic drugs are all associated with changes in markers of ER stress and ER-mediated cell death in vivo ... PubMed Abstract

Peyrou M et al; Toxicol Sci 99 (1): 346-53 (2007)

4-Aminophenol (4-AP), D-serine, and cisplatin are established rodent nephrotoxins that damage proximal tubules within the renal cortex ... High throughput 2D gel proteomics to profile protein changes in the plasma of compound-treated animals, ... /demonstrated/ several markers of kidney toxicity. Male F344 and Alpk rats were treated with increasing doses of 4-AP, D-serine, or cisplatin, and plasma samples were collected over time ... Several isoforms of the rat-specific T-kininogen protein were identified in each study. T-kininogen was elevated in the plasma of 4-AP-, D-serine-, and cisplatin-treated animals at early time points, returning to baseline levels 3 weeks after treatment. The protein was not elevated in the plasma of control animals or those treated with nontoxic compounds. /It was proposed/ that T-kininogen may be required to counteract apoptosis in proximal tubular cells in order to minimize tissue damage following a toxic insult. In addition, T-kininogen may be required to stimulate localized inflammation to aid tissue repair ... Several isoforms of the inter-alpha inhibitor H4P heavy chain /were identified/ in the 4-AP and D-serine studies. In each case, the protein expression levels in the blood samples paralleled the extent of kidney toxicity, highlighting the correlation between protein alterations and clinical chemistry endpoints. A further set of proteins correlating with kidney damage was found to be a component of the complement cascade and other blood clotting factors, indicating a contribution of the immune system to the observed toxicity. These observations underscore the value of proteomics in identifying new biomarkers and in the elucidation of mechanisms of toxicity. PubMed Abstract

Bandara LR et al; Toxicol Sci 73 (1): 195-206 (2003)

One of the primary effects found from exposure to p-aminophenol is the formation of methemoglobin. This effect has been found in many species with a wide degree of susceptibility. The oxidation of hemoglobin to methemoglobin interferes with normal oxygen transport functions of hemoglobin and can result in a chemical asphyxia (usually at levels of 60% or more). It is believed that p-aminophenol forms a covalent bond with the reactive -SH groups of hemoglobin and transfers electrons to oxygen to created methemoglobin.

European Commission, ESIS; IUCLID Dataset, 4-Aminophenol (123-30-8) p.43 (2000 CD-ROM edition). Available from, as of May 17, 2010:

p-Aminophenol is a significantly toxic chemical and one mechanism associated with its cytotoxicity has been attributed to its activity as a tissue respiratory (oxidative phosphorylation) inhibitor ... .

Clayton, G.D., F.E. Clayton (eds.) Patty's Industrial Hygiene and Toxicology. Volumes 2A, 2B, 2C, 2D, 2E, 2F: Toxicology. 4th ed. New York, NY: John Wiley & Sons Inc., 1993-1994., p. 973

Ask Us for Pharmaceutical Supplier and Partner
Ask Us, Find A Supplier / Partner
No Commissions, No Strings Attached, Get Connected for FREE

What are you looking for?

How can we help you?

The request can't be empty

Please read our Privacy Policy carefully

You must agree to the privacy policy

The name can't be empty
The company can't be empty.
The email can't be empty Please enter a valid email.
The mobile can't be empty

Advertise With Us

Advertise With Us