2 許多藥物發生 desensitization 的機轉為其受體被：
(A)磷酸化
(B)去磷酸化
(C)甲基化
(D)乙醯化

35 下列敘述何者正確？ 
(A) 致效劑（Agonist）與受體結合的Kd 值較拮抗劑（Antagonist）小 
(B) 拮抗劑具有與致效劑相反的逆向intrinsic activity 
(C) 作用強度（Potency）越大的藥物臨床療效越好 
(D) 活化劑的作用易產生脫敏反應（Desensitization） 

把接在受體上的荷爾蒙分解掉，其過程如下：
a.在細胞膜上已和ligand（就是荷爾蒙）結合的G蛋白偶合受體（G protein-couple receptor），會被GRK（G protein-couple receptor protein kinase）磷酸化，GRK會先接在受體上，把兩個磷酸根接在受體的偏細胞質側，當磷酸根接上後GRK會離開，而受體被磷酸化的地方提供了arrestin結合的位置
b.當arrestin與受體結合後，會促進細胞進行胞吞作用，將受體吞入細胞內形成內吞體（endosome），內吞體內的pH約3~6，如此偏酸的環境會破壞荷爾蒙（ligand）和受體的結合力，將兩者分開
c.從受體上脫離的荷爾蒙之後會由囊泡（vesicle）送入溶小體（lysosome）被降解掉，因為溶小體內含有許多水解酵素，而受體則會被去磷酸化（dephosphorylation）後，由另一個囊泡送回細胞膜上與細胞膜融合，受體因此可重複使用

rf:https://smallcollation.blogspot.com/2013/08/desensitization.html#gsc.tab=0 

Fig. 1. Homologous desensitization and trafficking of G-protein-coupled receptors mediated by GRKs and arrestins. The GPCR is activated by agonist (1) leading to G protein coupling (2) and effector modulation. The agonist-occupied GPCR is subsequently phosphorylated by GRK (3) and arrestin binds to the phosphorylated GPCR, leading to receptor desensitization (4) and internalization to endosomes (5). For most GPCRs, internalization following relatively short-term agonist treatment leads to dephosphorylation (6) and recycling (7) of the GPCR. Depending upon the GPCR subtype, arrestin either dissociates from the receptor at the plasma membrane or after co-internalization with the receptor (5). Particularly with longer agonist treatments, internalized GPCR may also be targeted for down-regulation (8). Newly synthesized receptor, or receptor stored in an intracellular pool, can also be inserted into the plasma membrane (9), although the factors that control this are poorly understood.

https://www.semanticscholar.org/paper/Adenosine-receptor-desensitization-and-trafficking.-Mundell-Kelly/ab26ccfb07322655ddc0b5c9dbcad5c5f68d7555/figure/0