## 1 Introduction  
Natural compounds can have their structures altered via conjugation with amino acids. Since amino acids are the fundamental monomers of living systems, they are selected for these modifications [1]. Furthermore, structural modification with a wider shift is possible because amino acids have different side chains [2]. Several conjugations of natural compounds with certain amino acids, especially glycine, show the expected biological response. Poly-R-(L-glutamic acid)-glycine-campothecin demonstrated good anticancer activity, reducing the development of B-16 cancer cells following 48 h of therapy at a lower dose [3]. Glycine-conjugated podophyllotoxin exhibited excellent anticancer efficacy against the MCF7 cell line, with an IC\({}_{50}\) of 7.2 nM [4]. Diglycinoyl curcumin demonstrated potent antitumor efficacy against the HeLa cell line [5]. It has been reported that the synthesis of glycyrrheinic acid-amino acid derivatives has been performed to boost their cytotoxic activity. Through esterification with benzyl ester, a modification was carried out at the C-30 position. It was discovered that glycine-conjugatedglycyrrhetinic acid was more effective than glycyrrhetinic acid in inhibiting the MCF7 cancer cell line, with an IC\({}_{50}\) of 3.8 uM compared to >40 uM for pure glycyrrhetinic acid [6]. Research on \(\alpha\)-magnostin, a compound found in _Garcinia mangostana_, has been conducted in the area of potential natural product intervention [7]. Previous research demonstrated that a mangosteen find extract exhibits cytotoxic action against MCF-7 breast cancer cells with an IC\({}_{50}\) value of 45 ug/mL, in addition to inducing apoptosis and changing the cells' morphology [8]. \(\alpha\)-Mangostin, which constitutes about 8-15% of the active ingredient in mangosteen, is primarily found in the pericarps of the plant [9]. The pharmacological activity of this chemical includes antibacterial [10], antioxidant, anti-inflammatory [11], and anticancer properties. Because of its natural [12] origin, \(\alpha\)-mangostin has a lower adverse effect profile than tamoxifen [13]. Tamoxifen is a selective estrogen receptor modulator commonly used to treat estrogen-receptor-positive breast cancer [14]. It works by inhibiting the growth and proliferation of breast cancer cells by blocking their estrogen receptors, but it has been linked to cardiovascular challenges [15]. \(\alpha\)-Mangostin has a more expansive mechanism of action, including antioxidant, anti-inflammatory, and antimetastatic effects, and can be effective in a variety of breast cancer types other than those that are ER-positive, indicating a potential for overcoming resistance due to its multiple mechanisms of action and ability to target cancer cells [16]. However, inadequate bioavailability was found in an \(\alpha\)-mangostin pharmacokinetic investigation conducted in mice [17]. Additionally, the cytotoxicity of tyrosine-conjugated chlorambucil is greater than that of chlorambucil alone due to its increased intracellular absorption. L-type amino acid transporter 1 (LAT1), which is overexpressed in a number of cancer types, enhances the antiproliferative activity of the chlorambucil compound and aids in its intracellular uptake [18]. It is overexpressed in a number of cancer types [19]. Interestingly, lysine, arginine, and histidine have been conjugated with the C3 and C6 atoms of \(\alpha\)-mangostin in an attempt to improve its selectivity against bacterial membranes [20]. In this study, glycine-conjugated \(\alpha\)-mangostin was designed to target the estrogen receptor. A considerable majority of breast cancers are hormone receptor-positive, meaning they express estrogen and/or progesterone receptors [21]. Estrogen stimulates the growth of these tumors by attaching to their receptors and increasing gene expression, leading to cell proliferation [22].