3,7-Dimethyl-9-(2,6,6-trimethylcyclohex-1-en-1-yl)nona-2,4,6,8-tetraenoic acid

식별자 및 물리적 특성

분자식	C20H28O2
평균 분자량	300.4 g/mol
SMILES	CC(C=CC1=C(C)CCCC1(C)C)=CC=CC(C)=CC(=O)O
InChIKey	SHGAZHPCJJPHSC-UHFFFAOYSA-N
PubChem CID	5538
ChEMBL	CHEMBL1235644
ChEBI	CHEBI:26536

화학 및 물리적 성질

XLogP	6.3
극성 표면적	37.3
수소 결합 공여자 수	1
수소 결합 수용자 수	2
회전 가능 결합 수	5
무거운 원자 수	22
형식 전하	0
복잡도	567
LogP(분배 계수)	6.3

안전 및 규제

노출 경로	1-31% (topical)
독성 요약	Tretinoin binds to alpha, beta, and gamma retinoic acid receptors (RARs). RAR-alpha and RAR-beta have been associated with the development of acute promyelocytic leukemia and squamous cell cancers, respectively. RAR-gamma is associated with retinoid effects on mucocutaneous tissues and bone. Although the exact mechanism of action of tretinoin is unknown, current evidence suggests that the effectiveness of tretinoin in acne is due primarily to its ability to modify abnormal follicular keratinization. Comedones form in follicles with an excess of keratinized epithelial cells. Tretinoin promotes detachment of cornified cells and the enhanced shedding of corneocytes from the follicle. By increasing the mitotic activity of follicular epithelia, tretinoin also increases the turnover rate of thin, loosely-adherent corneocytes. Through these actions, the comedo contents are extruded and the formation of the microcomedo, the precursor lesion of acne vulgaris, is reduced. Tretinoin is not a cytolytic agent but instead induces cytodifferentiation and decreased proliferation of APL cells in culture and in vivo. When Tretinoin is given systemically to APL patients, tretinoin treatment produces an initial maturation of the primitive promyelocytes derived from the leukemic clone, followed by a repopulation of the bone marrow and peripheral blood by normal, polyclonal hematopoietic cells in patients achieving complete remission (CR). The exact mechanism of action of tretinoin in APL is unknown.
Carcinogen Classification	No indication of carcinogenicity to humans (not listed by IARC).

분자식

C20H28O2

평균 분자량

300.4 g/mol

SMILES

CC(C=CC1=C(C)CCCC1(C)C)=CC=CC(C)=CC(=O)O

InChIKey

SHGAZHPCJJPHSC-UHFFFAOYSA-N

PubChem CID

5538

ChEMBL

CHEMBL1235644

ChEBI

CHEBI:26536

XLogP

6.3

극성 표면적

37.3

수소 결합 공여자 수

수소 결합 수용자 수

회전 가능 결합 수

무거운 원자 수

형식 전하

복잡도

567

LogP(분배 계수)

6.3

안전 및 규제

노출 경로

1-31% (topical)

독성 요약

Tretinoin binds to alpha, beta, and gamma retinoic acid receptors (RARs). RAR-alpha and RAR-beta have been associated with the development of acute promyelocytic leukemia and squamous cell cancers, respectively. RAR-gamma is associated with retinoid effects on mucocutaneous tissues and bone. Although the exact mechanism of action of tretinoin is unknown, current evidence suggests that the effectiveness of tretinoin in acne is due primarily to its ability to modify abnormal follicular keratinization. Comedones form in follicles with an excess of keratinized epithelial cells. Tretinoin promotes detachment of cornified cells and the enhanced shedding of corneocytes from the follicle. By increasing the mitotic activity of follicular epithelia, tretinoin also increases the turnover rate of thin, loosely-adherent corneocytes. Through these actions, the comedo contents are extruded and the formation of the microcomedo, the precursor lesion of acne vulgaris, is reduced. Tretinoin is not a cytolytic agent but instead induces cytodifferentiation and decreased proliferation of APL cells in culture and in vivo. When Tretinoin is given systemically to APL patients, tretinoin treatment produces an initial maturation of the primitive promyelocytes derived from the leukemic clone, followed by a repopulation of the bone marrow and peripheral blood by normal, polyclonal hematopoietic cells in patients achieving complete remission (CR). The exact mechanism of action of tretinoin in APL is unknown.

Carcinogen Classification

No indication of carcinogenicity to humans (not listed by IARC).