Panitumumab

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Panitumumab?
Therapeutic monoclonal antibody
Source	Human recombinant
Target	EGFR
Identifiers
CAS number	339177-26-3
ATC code	L01XC08
PubChem	?
Chemical data
Formula	C6306H9732N1672O1994S46
Mol. mass	?
Pharmacokinetic data
Bioavailability	?
Metabolism	?
Half life	∼7.5 days (range: 4-11 days)
Excretion	?
Therapeutic considerations
Pregnancy cat.	?
Legal status	℞ Prescription only
Routes	intravenous

Panitumumab (ABX-EGF) is a fully human monoclonal antibody specific to the EGF receptor (see illustration)[2].

Panitumumab is manufactured by Amgen and marketed as Vectibix.

Contents 1 Uses 2 Mechanism 3 Production 4 Panitumumab vs. cetuximab 5 References 6 Further reading

[edit] Uses

It was FDA approved for the first time in September 2006, for the "the treatment of EGFR-expressing metastatic colorectal cancer with disease progression" despite prior treatment ^[1]. Panitumumab was approved by the European Medicines Agency (EMA) on December 3, 2007. Research showed that panitumumab is only effective in patients having the wild type of KRAS gene.

[edit] Mechanism

The compound works by binding to the extracellular domain of the EGFR (epidermal growth factor receptor) preventing its activation. This in turn, results in halting of the cascade of intracellular signals dependent on this receptor. ^[2]

[edit] Production

Panitumumab is produced by immunization of transgenic mice (xenomouse), that are able to produce human immunoglobulin light and heavy chains. After immunization of these animals a specific clone of B cells that produced an antibody against EGFR was selected and immortalized in Chinese hamster ovary (CHO) cells. These cells are then used for the full scale manufacture of the antibody.

[edit] Panitumumab vs. cetuximab

Although they both target the EGFR, panitumumab (IgG2) and cetuximab (IgG1) differ in their isotype and they might differ in their mechanism of action. Monoclonal antibodies of the IgG1 isotype may activate the complement pathway and mediate ADCC (antibody-dependent cellular cytotoxicity) better than their IgG2 counterparts, hence although they have not been documented, differences in the responses in treatments with these two antibodies might be expected. ^[3]

[edit] References

[edit] Further reading

Philippe Rougier, Emmanuel Mitry, Sophie Dominguez. Les Cancers Digestifs ; Springer , September 1, 2006, page=291 ; language=French

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