Cyclophosphamide (NSC-26271) Monohydrate

For research use only.

Catalog No.S2057

24 publications

Cyclophosphamide (NSC-26271) Monohydrate Chemical Structure

CAS No. 6055-19-2

Cyclophosphamide (NSC-26271) Monohydrate is a nitrogen mustard alkylating agent, it attaches the alkyl group to the guanine base of DNA, shown to crosslink DNA, causing strand breakage and inducing mutations.

Selleck's Cyclophosphamide (NSC-26271) Monohydrate has been cited by 24 publications

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Biological Activity

Description Cyclophosphamide (NSC-26271) Monohydrate is a nitrogen mustard alkylating agent, it attaches the alkyl group to the guanine base of DNA, shown to crosslink DNA, causing strand breakage and inducing mutations.
In vitro

Cyclophosphamide (CY) is a chemotherapeutic agent with a dose-dependent, bimodal effect on the immune system. Cyclophosphamide treatment enhances apoptosis and decreases homeostatic proliferation of regulatory T cells. Cyclophosphamide downregulates the expression of GITR and FoxP3, which are involved in the suppressive activity of T(REGs).[1] Cyclophosphamide increases CYP3A4, CYP2C8, and CYP2C9 protein levels in primary human hepatocyte cultures, which thereby enhances their own rates of 4-hydroxylation in the cultured hepatocytes. [2] Cyclophosphamide has produced mutations in base-pair substituting strains of Salmonella tryphimurium in the presence of metabolic activation, but it has been shown to be negative in the E. coli chromotest. Cyclophosphamide has been shown to produce gene mutations, chromosome aberrations, micronuclei and sister chromatid exchanges in a variety of cultured cells in the presence of metabolic activation as well as sister chromatid exchanges without metabolic activation. [3]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
BALB/c 3T3 cells NFzj[2VEgXSxdH;4bYNqfHliYYPzZZk> Mo\HTY4hfmm2cn:gZ5l1d3SxeHnjbZR6KHejczDleoFtfWG2ZXSgbY4hdW:3c3Wg[Y1jenmxIFLBUGIw[yB|VEOgZ4VtdHNuIFnDOVA:OzdwNjFOwG0> MXm8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:ydXLt[YQvdmOkaT7ucI0vdmmqLnfvek86QDd|NEGyK|46QDd|NEGyQE9iRg>?
HL60 cells MkHCR5l1d3SxeHnjbZR6KGG|c3H5 NWPq[3RsS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hUEx4MDDj[YxteyCkeTDNWHQh[XO|YYmsJGlEPTB;OD63PUDPxE1? NXXleYo1RGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC|Oj:vdJVjdWWmLn7jZokvdmyvLn7pbE5od3ZxMkC4OVA{ODNpPkKwPFUxOzB|PD;hQi=>
BALB/c 3T3 MYrDfZRwfG:6aXPpeJkh[XO|YYm= NFm3do9KdiC4aYTyc{BkgXSxdH;4bYNqfHliYXfhbY5{fCCEQVzCM4MhO1R|IHPlcIx{NCCLQ{WwJF0hOzdwNjFOwG0v MWS8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:ydXLt[YQvdmOkaT7ucI0vdmmqLnfvek84QDd5MUWwK|44QDd5MUWwQE9iRg>?
T-cells M{DzdGludXWwb4P1dJBz\XO|aY\lJIF{e2G7 NFjSXJkyODBibXevb4c> M3K3b|gh\GG7cx?= MoXDTY1ufW6xc4XwdJJme3OrdnWgZYN1cX[rdImgZYdicW6|dDDNRXYuOSCrbn\lZ5Rm\CCEQVzCM4MhdW:3c3WgZZN{\XO|ZXSgZZMhXCClZXzsd{B{fXCycnXzd4lwdiCjdDCxNFAhdWdxa3esJIlxKHS{ZXH0[YQhQCCmYYnzJIJm\m:{ZTDpcoZm[3Srb36g[o9zKDRid3Xlb5MhdWWjc4Xy[YQhOTRiZHH5d{Bxd3O2IHnu[oVkfGmxbjDifUBndG:5IHP5eI9u\XS{eR?= MXS8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:ydXLt[YQvdmOkaT7ucI0vdmmqLnfvek8yQDJ4OEC4OUc,OTh{NkiwPFU9N2F-
B-cells NWjveYwxUW2vdX7vd5VxeHKnc4PpeoUh[XO|YYm= NFPnR5oyODBibXevb4c> MlnrPEBl[Xm| MYDJcY12dm:|dYDwdoV{e2m4ZTDhZ5Rqfmm2eTDh[4FqdnO2IF3BWk0yKGmwZnXjeIVlKEKDTFKvZ{Bud3W|ZTDhd5Nme3OnZDDhd{BDKGOnbHzzJJN2eHC{ZYPzbY9vKGG2IEGwNEBu\y:tZzygbZAhfHKnYYTl[EA5KGSjeYOgZoVnd3KnIHnu[oVkfGmxbjDmc5IhPCC5ZXXrd{Bu\WG|dYLl[EAyPCCmYYnzJJBwe3RiaX7m[YN1cW:wIHL5JIZtd3diY4n0c41mfHK7 NGnL[XY9[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;weYJu\WRwbnPibU5vdG1wbnnoModwfi9zOEK2PFA5PSd-MUiyOlgxQDV:L3G+
U87 MG NUT2cpI3SW62aYT1cY9zKGG|c3H5 MUe4NEBu\y:tZx?= MXrBcpRqfHWvb4KgZYN1cX[rdImgbY4hcHWvYX6gWVg4KE2JIHPlcIx{KHinbn;ndoFnfGWmIH3veZNmKGG2IEiwJI1oN2upLDDpekBi\G2rbnnzeIVz\WRiaX6gVVJFKHhiNTDzZ4hm\HWuZR?= NWH4XlJ1RGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC|Oj:vdJVjdWWmLn7jZokvdmyvLn7pbE5od3ZxMUi0OVA1PTZpPkG4OFUxPDV4PD;hQi=>
MX1 MoHQRY51cXS3bX;yJIF{e2G7 M3\ZWFEzOCCvZz;r[y=> NH7jSI52eCC2bzCzJJdm\Wu| MX7BcpRqfHWvb4KgZYN1cX[rdImgZYdicW6|dDDoeY1idiCPWEGgZ4VtdHNieHXuc4dz[W[2ZXSgbY4hdnWmZTDtc5V{\SCjZHr1eoFvfCCvb3TlcEBie3Onc4Pl[EBieyCrbnPy[YF{\SCrbjDtc5V{\SC|dYL2bZZidCC2aX3lJIF1KDF{MDDt[{9s\yxicH:gRmlFKG2nYYP1doVlKHWyIITvJFMhf2Wna4O= NGLBOWs9[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;weYJu\WRwbnPibU5vdG1wbnnoModwfi9{MEeyOlUyOid-MkC3NlY2OTJ:L3G+
U87MG NF\LUJVCdnSrY3HuZ4VzKGG|c3H5 MoLwPFAhdWdxa3e= NIfyPWo3KGSjeYO= M1e5UWFvfGmlYX7j[ZIh[WO2aY\peJkh[WejaX7zeEBpfW2jbjDVPFdOTyClZXzsd{B5\W6xZ4Lh[pRm\CCrbjDheIh6dWmlIH3veZNmKGG|c3Xzd4VlKGG|IIT1cY9zKHO3cIDy[ZN{cW:wIHH0JFgxKG2pL3vnMEBqfiCTMlSg[o9zKDZiZHH5dy=> M3\JWFxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4D1Zo1m\C6wY3LpMo5tdS6waXiu[493NzJzMUC2N|c4Lz5{MUGwOlM4PzxxYU6=
NCI-H522 MWnBcpRqfHWvb4KgZZN{[Xl? NGjqUWs2OCCvZz;r[y=> MoH0Nlgh\GG7cx?= NVvxRYdbSW62aYT1cY9zKGGldHn2bZR6KGGpYXnud5QhcHWvYX6gUmNKNUh3MkKgZ4VtdHNieHXuc4dz[W[2ZXSgbY4hSmGuYj;jJI52\GVibX;1d4Uh[XO|ZYPz[YQh[XNidIXtc5Ih\3Kxd4ToJIlvcGmkaYTpc44h[XRiNUCgcYcwc2duIHnnJIFldWmwaYP0[ZJm\CCxbnPlJIRicWy7IH\vdkAzQCCmYYnzJJJmdGG2aY\lJJRwKGOxboTyc4w> MnuwQIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xcIXicYVlNm6lYnmucoxuNm6raD7nc5YwOjhyOUK4OlAoRjJ6MEmyPFYxRC:jPh?=
U2932 NVXtRlBGSW62aYT1cY9zKGG|c3H5 NI[1Z|U2OCCvZz;r[y=> MnTqOUBkd26|ZXP1eIl3\SCmYYnz NXu5cnBkSW62aYT1cY9zKGGldHn2bZR6KGGpYXnud5QhcHWvYX6gWVI6OzJiY3XscJMhgGWwb3fyZYZ1\WRiaX6gV2NKTCCvb4Xz[UBie3Onc4Pl[EBieyC{ZXT1Z5Rqd25iaX6geJVud3JiYoXy[IVvKGG2IEWwJI1oN2upLDDpdEBi\G2rbnnzeIVz\WRiZn;yJFUh[2:wc3XjeZRqfmViZHH5d{Bu\WG|dYLl[EB2eCC2bzDkZZkhPDBicH;zeEBk\WyuIHnuboVkfGmxbh?= NILRfnE9[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;weYJu\WRwbnPibU5vdG1wbnnoModwfi9{OE[wOVU6Oyd-Mki2NFU2QTN:L3G+
MDA-MB-231 NIL2eW1EgXSxdH;4bYNqfHliYYPzZZk> M{SwdVQ5KGi{ NF\PW41EgXSxdH;4bYNqfHliYXfhbY5{fCCKb33vJJNieGmnboOgLIh2dWGwKTDNSGEuVUJvMkOxJINmdGy|IHHmeIVzKDR6IHjyJIJ6KE2WVDDhd5NigSxiSVO1NEA:KDBwMEmg{txONg>? MVO8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:5d4eu[YJqNmGlLoXrM4Np\W2kbD;jc41xd3WwZG;y[ZBwenShY3Hy[E9EUEWPQly4PE8oRkOqRV3CUFww[T5?
K562 NIrmbFBEgXSxdH;4bYNqfHliYYPzZZk> MkniOFghcHJ? NIToe4hEgXSxdH;4bYNqfHliYXfhbY5{fCCKb33vJJNieGmnboOgLIh2dWGwKTDLOVYzKGOnbHzzJIFnfGW{IES4JIhzKGK7IF3UWEBie3OjeTygTWM2OCB;IECuNVUh|ryPLh?= MYG8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:5d4eu[YJqNmGlLoXrM4Np\W2kbD;jc41xd3WwZG;y[ZBwenShY3Hy[E9EUEWPQly4PE8oRkOqRV3CUFww[T5?
K562 MWXBcpRqeHKxbHnm[ZJifGm4ZTDhd5NigQ>? M3zrWFQ5KGi{ NH;jemtCdnSrcILvcIln\XKjdHn2[UBi[3Srdnn0fUBi\2GrboP0JGhwdW9ic3HwbYVveyBqaIXtZY4qKEt3NkKgZ4VtdHNiYX\0[ZIhPDhiaIKgZpkhVVSWIHHzd4F6NCCLQ{WwJF0hOC5zNUOg{txONg>? MlTSQIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xd4f3MoVjcS6jYz71b{9kcGWvYnyvZ49ueG:3bnTfdoVxd3K2X3PhdoQwS0iHTVLMPFgwLz6FaFXNRmw9N2F-
MCF7 MmC1R5l1d3SxeHnjbZR6KGG|c3H5 NEDSO4E1QCCqch?= NITBdVVEgXSxdH;4bYNqfHliYXfhbY5{fCCKb33vJJNieGmnboOgLIh2dWGwKTDNR2Y4KGOnbHzzJIFnfGW{IES4JIhzKGK7IITyfZBidiCkbIXlJIF{e2G7LDDJR|UxKD1iMD6xOkDPxE1w NInmbpo9[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;3e5cv\WKrLnHjMpVsN2OqZX3icE9kd22yb4Xu[H9z\XCxcoTfZ4Fz\C:FSFXNRmw5QC9pPlPoSW1DVDxxYU6=
HepG2 NYfOOnE5S3m2b4TvfIlkcXS7IHHzd4F6 NUDLPY5lPDhiaIK= MYXDfZRwfG:6aXPpeJkh[WejaX7zeEBJd22xIIPhdIlmdnNiKHj1cYFvMSCKZYDHNkBk\WyuczDh[pRmeiB2ODDodkBjgSCPVGSgZZN{[XluIFnDOVAhRSByLkK0JO69VS5? NETDW|g9[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;3e5cv\WKrLnHjMpVsN2OqZX3icE9kd22yb4Xu[H9z\XCxcoTfZ4Fz\C:FSFXNRmw5QC9pPlPoSW1DVDxxYU6=

... Click to View More Cell Line Experimental Data

Assay
Methods Test Index PMID
Western blot
PTEN / pAkt / Caspase 3 / GAPDH; 

PubMed: 23874108     


Western blotting revealed different protein expression in all four intervention groups relative to that in the control group. PTEN and caspase 3 were increased after treatment with cyclophosphamide and/or Chalone 19-peptide. pAkt expression was decreased in the treatment group.

Caspase 3 / Cleaved-Caspase 3 / Cleaved-PARP / Tubulin; 

PubMed: 31429028     


AURKA inhibition induces caspase-independent apoptosis. (a) Induction of caspase-3 and PARP cleavage by immunoblotting in Raji cells treated with PBS (negative control), cyclophosphamide, MLN8237, combination of cyclophosphamide and MLN8237, or etoposide (positive control) at 24 hours.

Nuclear AIF / Cytosolic AIF / TBP / GAPDH; 

PubMed: 31429028     


AURKA inhibition induces caspase-independent apoptosis. (c) Cytosolic and nuclear AIF levels over time in Raji cells treated with MLN8237 at 8, 16, and 24 hours.

LC3B I / LC3B II / GAPDH; 

PubMed: 31429028     


AURKA inhibition reverses autophagy. (a) LC3B-II levels by immunoblotting in chemoresistant (Raji) cells treated with PBS (negative control), cyclophosphamide, MLN8237, or combination of cyclophosphamide and MLN8237, or etoposide (positive control) at 48 hours.

23874108 31429028
Growth inhibition assay
Cell Viability; 

PubMed: 31429028     


Baseline characteristics of chemosensitive (Ramos) and chemoresistant (Raji) Myc-positive cell lines. (c) Cytotoxicity assay of cyclophosphamide, MLN8237, or the combination in chemoresistant Raji cells.

Tumor Volume; 

PubMed: 24681847     


(B–C) MUC1.Tg mice bearing (B) MC38/MUC1+ s.c. tumors or (C) Panc02/MUC1+ orthotopic tumors were randomized and treated with control liposomes, cyclophosphamide and tecemotide, cyclophosphamide and NHS-muIL12, or the combination of cyclophosphamide, tecemotide, and NHS-muIL12 (n = 9-10 mice per group).

Tumor Volume; 

PubMed: 21069336     


In vivo antitumour activity of the combination of fisetin with cyclophosphamide. Twenty mice bearing bilateral Lewis lung tumours were randomly assigned to four groups of 5 mice as follows: control, solvent alone (squares); fisetin, 223 mg/kg i.p. on days 4 to 8 and days 11, 12, 14 (triangles); cyclophosphamide, 30 mg/kg s.c., on days 4, 5, 7, 8 (diamonds); and, the combination of cyclophosphamide and fisetin (solid circles), both administered at the same dose and schedule when used alone. Tumour volumes were determined as described in Materials and Methods. Mean ± SEM.

31429028 24681847 21069336
IHC
tumor cell invasion; 

PubMed: 23874108     


(A) Animal model control group with tumor cell wear through skin squamous epithelium, HE × 120. (B) Animal model control group with tumor cell invasion to skeletal muscles, HE × 120. (C) Animal model control group with tumor cells actively around blood vessels, HE × 120. (D) Animal model control group showing pulmonary metastasis, HE × 460. (E) Cyclophosphamide group with hemorrhage and necrotic tissue in liver, HE × 460. (F) Chalone 19-peptide group showing hydropic degeneration in hepatic cells, HE × 460. (G) Cyclophosphamide 100 mg/kg and Chalone 19-peptide combined treatment group showing fatty degeneration of tumor cells, HE × 460. (H) Cyclophosphamide 50 mg/kg and Chalone 19-peptide combination treatment group showing punctuate phagocytic infiltration, HE × 460. (I) Control group with slight phagocytic infiltration, HE × 460.

TUNEL / Caspase 3; 

PubMed: 23874108     


TUNEL analysis and immunohistochemistry testing of caspase 3 showing apoptosis in all four intervention groups relative to controls. (A) Immunohistochemistry testing of caspase 3. (a1) Cyclophosphamide group, (a2) Chalone 19-peptide group, (a3) Cyclophosphamide 100 mg/kg and Chalone 19-peptide combined treatment group, (a4) Cyclophosphamide 50 mg/kg and Chalone 19-peptide combined treatment group, and (a5) control group (×460). (B) Immunofluorescence testing of TUNEL. (b1) Cyclophosphamide group, (b2) Chalone 19-peptide group, (b3) Cyclophosphamide 100 mg/kg and Chalone 19-peptide combined treatment group, (b4) Cyclophosphamide 50 mg/kg and Chalone 19-peptide combined treatment group, and (b5) control group (×460). (C) Immunohistochemistry testing of TUNEL. (c1) Cyclophosphamide group, (c2) Chalone 19-peptide group, (c3) Cyclophosphamide 100 mg/kg and Chalone 19-peptide combined treatment group, (c4) Cyclophosphamide 50 mg/kg and Chalone 19-peptide combined treatment group, and (c5) control group (×460).

PTEN / pAkt / PCNA; 

PubMed: 23874108     


Immunohistochemistry revealing different proteins in intervention groups relative to controls. Micrographs of cells after immunohistochemistry showing that PTEN, pAKt, and proliferating cells were produced by the different groups. After treatment with cyclophosphamide and/or Chalone 19-peptide, PTEN was increased. pAkt and PCNA were decreased and necrosis was observed (×460). (A) Immunohistochemistry testing of PTEN. (a1) Cyclophosphamide group, (a2) Chalone 19-peptide group, (a3) Cyclophosphamide 100 mg/kg and Chalone 19-peptide combined treatment, (a4) Cyclophosphamide 50 mg/kg and Chalone 19-peptide combined treatment group, and (a5) control group. (B) Immunohistochemistry testing of pAkt. (b1) Cyclophosphamide group, (b2) Chalone 19-peptide group, (b3) Cyclophosphamide 100 mg/kg and Chalone 19-peptide combined treatment group, (b4) Cyclophosphamide 50 mg/kg and Chalone 19-peptide combined treatment group, and (b5) control group. (C) Immunohistochemistry testing of PCNA. (c1) Cyclophosphamide group, (c2) Chalone 19-peptide group, (c3) Cyclophosphamide 100 mg/kg and Chalone 19-peptide combined treatment group, (c4) Cyclophosphamide 50 mg/kg and Chalone 19-peptide combined treatment group, and (c5) control group.

ovary of mice; 

PubMed: 32308430     


The effect of testosterone in mice treated with cyclophosphamide. Notes: (A) H&E staining of the ovary of mice treated with phosphate-buffered saline (PBS), cyclophosphamide (CPA) and cyclophosphamide plus testosterone (Ts). There are abundant primordial follicles (black arrows) and a few atresia (white arrows) in the ovaries of PBS-treated mice. In contrast, there are many atresia (white arrows) in the ovaries of CPA-treated mice. A small number of primordial follicles (black arrows) were found. In the ovaries of CPA plus Ts-treated mice, abundant primordial follicles (black arrows) and a few atresia (white arrows) were found. Bar = 100 μm.

Caspase-3; 

PubMed: 32308430     


The immunohistochemical analysis of cleaved Caspase-3 in mouse ovary. Notes: (A) The expression of cleaved-caspase-3 (Cl-Caspase-3) on immunohistochemistry. There are many follicles in mouse ovaries (black arrows). A large number of Cleave caspase-3-positive cells (white arrows) were found in the follicles of cyclophosphamide (CPA)-treated mice. In contrast, there were fewer Cl-Caspase-3 positive cells in the follicles in phosphate-buffered saline (PBS)-treated mice and cyclophosphamide plus testosterone (Ts)-treated mice. Bar = 100 μm.

23874108 32308430
Immunofluorescence
pAKT / pERK; 

PubMed: 31654636     


Representative images of phosphorylated AKT (pAKT) and phosphorylated extracellular signal-regulated kinase (pERK) immunostaining in keratinocyte growth factor (KGF)–pretreated bladders 1 day after cyclophosphamide injection.

Ki-67 / UPK3 / KRT5 / pERK; 

PubMed: 31654636     


Representative images and graphs of urothelial proliferation and phosphorylated extracellular signal-regulated kinase (pERK) immunostaining in keratinocyte growth factor (KGF)–pretreated bladders 6 hours after cyclophosphamide injection.

Ki-67 / KRT14 / KRT5; 

PubMed: 31654636     


Representative images and graphs of urothelial proliferation in keratinocyte growth factor (KGF)–pretreated bladders 1 day after cyclophosphamide injection.

autophagy levels; 

PubMed: 31429028     


(c) Representative photomicrograph (400 X) of autophagy levels in Raji cells stained with after treatment acridine orange staining with PBS (negative control), cyclophosphamide, MLN8237, or combination of cyclophosphamide and MLN8237. The accumulation of acidic vesicular organelles, which emit bright red/orange fluorescence correspond to autophagy activity.

31654636 31429028
In vivo Cyclophosphamide has also produced chromosome damage and micronuclei in rats, mice and Chinese hamsters, and gene mutations in the mouse spot test and in the transgenic lacZ construct of Muta Mouse. [3] Cyclophosphamide, when given in a defined sequence with a GM-CSF-secreting, neu-expressing whole-cell vaccine, enhances the vaccine's potential to delay tumor growth in neu transgenic mice. Cyclophosphamide mediates its effects by enhancing the efficacy of the vaccine rather than via a direct cytolytic effect on cancer cells. [4]

Protocol

Solubility (25°C)

In vitro DMSO 55 mg/mL (197.06 mM)
Water 7 mg/mL (25.08 mM)
Ethanol Insoluble

* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 279.1
Formula

C7H15Cl2N2O2P.H2O

CAS No. 6055-19-2
Storage powder
in solvent
Synonyms N/A
Smiles C1CNP(=O)(OC1)N(CCCl)CCCl.O

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Clinical Trial Information

NCT Number Recruitment interventions Conditions Sponsor/Collaborators Start Date Phases
NCT04757337 Recruiting Drug: Doxorubicin|Drug: Cyclophosphamide Advanced Soft-tissue Sarcoma|Metastatic Soft-tissue Sarcoma UNICANCER July 2021 Phase 3
NCT04656951 Recruiting Drug: Daratumumab Multiple Myeloma University of Cologne|Janssen-Cilag G.m.b.H June 1 2021 Phase 2

Tech Support

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Frequently Asked Questions

  • Question 1:

    Why S2057 Cyclophosphamide Monohydrate shows no activity in vitro assays?

  • Answer:

    Cyclophoshamide is a prodrug and needs Pytochrome P450 to convert it to the active form: 4-hydroxy cyclophosphamide. It is widely used in vivo, if you are going to use it in vitro, you'll have to supplement Pytochrome P450 exogenously.

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID